Ø Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants.
Ø The prevalence of TRVT is higher in deceased-donor than in living donor transplant. This may be because living-donor transplant procedures are usually done under more favourable conditions and are not usually subjected to ischemic injury.
Ø The Pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
Ø Causes of transplant renal vein thrombosis:
donor risk factors:
1. Older age of donors
2. Use of a donor’s right kidney is associated with the development of renal graft thrombosis due to the short vein and long artery of the right kidney.
3. Multiple graft vessels
4. Prolonged ischemia time
Recipient-related risk factors:
1. extremes of age
2. variations in vessel sizes between the donor and recipient
3. pretransplant dialysis modality
4. hypercoagulable states
Technical issues:
1. kinking of the graft vein, a long vein, wide disparities in vessel size
2. and injury to the vascular endothelium during surgical manipulation
Immunosuppression: administration of prothrombotic drugs such as cyclosporine, OKT3 antibody
Ø Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial wave – form positive during systole and negative during diastole), a spike-like systolic component, and non-visualization of the renal vein
Ø Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications. Magnetic resonance angiography is increasingly used to screen for vascular abnormalities in renal allografts
Ø Management of transplant renal vein thrombosis: Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical management of vascular complications must include surgical exploration of the allograft.
Ø Preventive strategies Because graft thrombosis is difficult to treat and graft loss is the usual outcome, development of preventive strategies is of paramount importance. First, technical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT.
Level 5
Ghalia sawaf
2 years ago
Causes of transplant renal vein thrombosis
often multifactorial and includes
• donor factors,
• recipient factors,
• technical issues during transplant surged (operative factors),
• and immunosuppression.
• donor risk factors,
1. short vein
2. long artery of the right kidney.
3. multiple renal arteries
4. prolonged ischemia timely
5. and vascular injuries
• Recipient-related risk factors
1. include extremes of age,
2. atherosclerotic vessels
3. variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures
4. peritoneal dialysis
5. antiphospholipid antibody syndrome,
6. antithrombin deficiency,
7. mutation of factor V Leiden,
8. the prothrombin gene.
9. Perioperative hemodynamic status, hypotension and dehydration
10. disease such as membranous nephropathy
A variety of technical issues
kinking of the graft vein,
a long vein,
abide disparities in vessel size,
injury to the vascular endothelium during surgical manipulation.
the most common causa of TRVT:
1. a kink in the renal vein,
2. compression by hematomas or lymphoceles,
3. anastomotic stenosis,
4. and extension of an underlying deep venous thrombosis.
5. compression of the renal vein by the renal artery, especially in contralateral transplant procedures (right kidney into the left iliac fossa and left kidney into the right iliac fossa).
6. Regarding immunosuppression, cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti- thymocyte/ antilymphocyte globulin.
Clinical manifestations
• The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
• Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur
• Transplant renal vein thrombosis may be complicated by pulmonary embolism,
Differential diagnosis
urologic complication or acute rejection, the most frequent complications during the early post-operative period.
Diagnosis of transplant renal vein thrombosis
a highly suspicious clinical presentation, triggering assessment using duplex ultrasonography
1. It characteristically reveals reversed arterial diastolic flow (ie, the arterial wave- form positive during systole and negative during diastole),
2. a spike-like systolic component,
3. and nonvisualization of the renal vein
Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels.
This high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss
The reversed diastolic wave form was described (in the main or segmental renal arteries), when retrograde blood flow occurred at any time point during the diastole, regardless of whether antegrade flow has happened.
There are 3 typical shapes of reversed diastolic wave form:
type I or “transient” wave form,
the revered diastolic wave form returns to baseline before end diastole;
type 2 or “plateau” waveform,
in which a flat reversed blots remains relatively constant throughout diastole;
and type 3 or “inverted M waveform , in which reversed flow throughout diastole has mid-diastolic deceleration.
A finding of isolated reversed or absent diastolic arterial flogs is sensitive and not pathognomonic and nonspecific to TRVT and may also be seen in
1. severe acute ejection,
2. severe acute tubular necrosis.
3. hematoma.
4. vascular kink
Previous studies have described a plateau-like or inverted M wave form associated with TRVT.
Whereas reversal of flow that is limited to the early diastole has been seen with seven rejection or acute tubular necrosis of the graft.
On the other hand, Lockhart and associates, showed that all waveform types could be present in TRVT patients, and reversed diastolic wave form types were not specific for any cause.
The diagnostic capability of duplex is influenced by
1. the patient’s body habitus,
2. the availability of suitable acoustic windows,
3. the operator’s skill
angiography
remains the standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
nuclear medicine scintigraphy or magnetic resonance angiography,
offer excellent alternatives to the criterion standard with no nephrotoxicity and a greater sensitivity than ultrasonography.
MRI
is considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
MRA
is increasingly used to screen for vascular abnormalities in renal allografts
Due to fear of nephrogenic systemic fibrosis after gadolinium-based contrast agents in patients with decreased GFR, imaging modalities have been developed to view the vessels without intravenous contrast.
Limitations of MRI include
the inability to image patients with pacemakers, greater cost, lack of portability, and prolonged examination time.
Management of transplant renal vein thrombosis
1. Two strategies are available for: thrombolytic therapy
2. surgical thrombectomy.
Successful emergency surgical thrombectomy has been reported in the early posttransplant period.
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT, notably after the second week after transplant )case or cohort studies.), there are no large randomized controlled studies
Preventive strategies
First, technical issues seem to play a major role; therefore,
meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT.
Sufficient training in techniques of vascular anastomosis and graft recovery is critical
A long renal vein is considered a risk factor of thrombosis in the experience of the authors; they routinely shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
They prefer ipsilateral transplant whatever possible and also in cases of short renal vessels
Attention to intravascular volume status
Transesophageal Doppler has been used to monitor the fluid balance during the procedure
duplex monitoring during the early posttransplant period followed by timely intervention
Some transplant centers have used strict protocols for postoperative monitoring:
1. hourly measurement of urine output,
2. daily duplex ultrasonography scanning
3. and daily measurements of serum creatinine and electrolyte levels.
Low-dose aspirin and low-molecular-weight heparin may also have benefits
Level 5
Last edited 2 years ago by Ghalia sawaf
Mohamed Fouad
2 years ago
Transplant Renal Vein Thrombosis
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant with a reported prevalence of 0.1% to 4.2%. Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases. The prevalence of TRVT is higher in deceased-donor than in living donor. There are many predisposing factors related to donor, recipient, surgery, and immunosuppression, with mechanical factors being considered the most common causes of transplant renal vein thrombosis. The diagnosis of transplant renal vein thrombosis depends on a high index of clinical suspicion and duplex ultrasonographic scans. Although venography remains the criterion standard, this procedure is invasive and nephrotoxic, due to use of ionizing contrast agents and also due to exposure to ionizing radiation.
Causes of transplant renal vein thrombosis:
The pathogenesis of TRVT is multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
1-Donor factors as donor’s right kidney is associated with the development of renal graft thrombosis due to the short vein and long artery of the right kidney. The short renal vein can be easily compressed postoperatively by the kidney swelling due to ischemic damage, acute tubular necrosis, or urinary obstruction. The right kidney is more difficult to position, especially if multiple renal arteries are present and the long artery can be easily kinked. vascular injuries, The prolonged ischemia time could potentiate thrombogenicity of the endothelium.
2-Recipient factors include extremes of age which may call for more complex sur gical procedures, Other recipient-related risk factors include pretransplant dialysis modality in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene. Perioperative hemodynamic status in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis, and primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
3-Technical issues have also been implicated as risk factors of TRVT, including kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
4-Immunosuppression factors TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti – thymocyte/antilymphocyte globulin.
Clinical manifestations of transplant renal vein thrombosis
The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock. Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours because of platelet sequestration in the thrombus.
Management of transplant renal vein thrombosis Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical management of vascular complications must include surgical exploration of the allograft.
Hamdy Hegazy
2 years ago
Please summarize this article The main cause of early renal graft dysfunction is transplant renal vein thrombosis which is commonly seen with deceased donor kidneys because of more exposure to ischemic injury. TRVT causes: 1- Donor’s right short vein and long artery leads to easily compressed vein with bulky kidney and kinked artery. 2- Donor’s kidney with multiples vessels. 3- Donor with prolonged ischemia and vascular injury. 4- Donor old age. 5- Recipients with extremes of age. 6- Recipients on peritoneal dialysis more than those on hemodialysis. 7- Recipients with peri-operative hypotension. 8- Recipients primary renal disease. 9- Technical issues: kinked graft vein, long vein, disparities in vessel size, vascular endothelial injury, compression by hematoma or lymphocele or renal artery, extension of lower limb DVT. 10- Surgical issues. 11- Immunosuppression: Cyclosporine, OKT3 antibody, ATG. Clinical diagnosis: Acute TRVT: oligo-anuric graft failure +/- hematuria, painful graft that might rupture leading to hemorrhagic shock because of intra-abdominal bleeding. Chronic TRVT: asymptomatic +/- thrombocytopenia. Imaging: Duplex USS: reversed or absent arterial diastolic flow. CT-angiography: invasive and nephrotoxic. MRA: is reliable method unless contra-indicated because of pacemaker. Treatment: either thrombolytic therapy or surgical thrombectomy.
What is the level of evidence provided by this article? Level V
Ahmed Omran
2 years ago
Allograft vein thrombosis is serious problem in the context of kidney transplantation. It occurs early post operatively. Several factors are interplaying, related to donor or recipient, medication and operative procedure. Its incidence: 1-4.2%.
It can lead allograft loss and nephrectomy in almost all cases. Donors Risk factors:
– Harvesting right kidney: in case of long artery and short vein.
The short vein is vulnerable for consequent compression by swollen allograft secondary to ATN, ischemic and rejection supervene.
Right kidney is difficult to implant than the left one due to possible multiple renal arteries, and long artery could be kinked.
Prolonged cold ischemia time and vascular injury are found to potentiate risk of venous thrombosis. Old aged donors , due to hypotension and resulting reperfusion injury facilitate procoagulant status in atherosclerotic. Recipients Risk factors :
Extreme of age is a prominent risk factor due to size difference &atherosclerotic changes.
Of note, peritoneal dialysis is more prone for ARVT compare with hemodialysis patients.
Peri-operative hypotension and dehydration might lead to AKI ATN , hypo-perfusion and thrombosis .Membranous nephropathy is associated higher incidence.
Abdullah Raoof
2 years ago
Q1- Please summarise this article?
Transplant Renal Vein Thrombosis
Abstract
It is occurs early with prevalence of 0.1% to 4.2%. Associate with bad prognosis with graft loss in almost all cases. predisposing factors related to donor, recipient, surgery, immunosuppression, and mechanical factors is the most common causes.
The clinical manifestations is nonspecific and and should be put in differential diagnosis of urine leak, urinary obstruction, or severe acute rejection.
The diagnosis needs a high index of clinical suspicion and duplex ultrasonography scans. Venography is invasive and nephrotoxic. Treatment: thrombolytic therapy and surgical thrombectomy. The prognosis bad usually end by allograft nephrectomy because delay in diagnosis.
Introduction
postoperative vascular complications occur in 1% to 10% of transplanted operations .
The most common vascular complications include
1) transplant renal artery stenosis,
2) renal graft arterial or venous thrombosis,
3) arterial injury, ( arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas )
presentation is dramatic with early graft dysfunction after renal transplant.
Prevalence of 0.1% to 4.2 % of all transplants. The prevalence is higher in deceased-donor than in living
Donor transplant. Usually end by graft loss and nephrectomy in almost all cases.
Causes of transplant renal vein thrombosis:
When considering donor risk factors:
1) Use of a donor’s right kidney.
2) Multiple graft vessels .
3) Prolonged ischemia time.
4) Vascular injuries.
5) Older age of donors
Recipient-related risk factors include:
1) Extremes of age.
2) Variations in vessel sizes between the donor and recipient.
3) Pre transplant dialysis modality.
4) Peritoneal dialysis.
5) Hypercoagulable states.
6) Perioperative hemodynamic status (hypotension) and dehydration.
7) primary renal disease as membranous nephropathy.
A variety of technical issues:
1) A kink in the renal vein.
2) Compression by hematomas or lymphoceles.
3) Anastomotic stenosis.
4) Extension of an underlying deep venous thrombosis.
Regarding immunosuppression:
1) Prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methylprednisolone, and anti thymocyte / ant lymphocyte globulin.
2) Cyclosporine can increase the risk of graft thrombosis.
Clinical manifestations of transplant renal vein thrombosis:
Typical present as rapid onset of oliguria or a anuria , hematuria with graft dysfunction, and a painful swollen graft which may progress to rupture, hemorrhage and shock. Chronic vein thrombosis is usually asymptomatic. Thrombocytopenia may occur. This complication beside urologic complication and acute rejection are three important causes of early graft dysfunction. May be complicated by pulmonary embolism. Diagnosis of transplant renal vein thrombosis:
The diagnosis depend on
1) a highly suspicious clinical presentation.
2) triggering assessment using duplex ultrasonography.
Ultrasonography is influenced by
1) The patient’s body habitus.
2) The availability of suitable acoustic windows.
3) The operator’s skill.
Angiography remains the criterion standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
Nuclear medicine scintigraphy or magnetic resonance angiography, are alternatives to the criterion standard with no nephrotoxicity and a greater sensitivity than ultrasonography.
MRI is now considered reliable tool for evaluation of renal allografts and the diagnoses of most complications. Because of nephrogenic systemic fibrosis ( gadolinium induced) imaging modalities have been developed to view the vessels without intravenous contrast.
Limitations of magnetic resonance imaging include
1) The inability to image patients with pace makers.
2) Greater cost.
3) lack of portability.
4) Prolonged examination time.
Management of transplant renal vein thrombosis:
Two treatment strategies are available:
1) Thrombolytic therapy.
2) Surgical thrombectomy.
Operative interventions gives better evaluation of the cause of thrombosis and can allow for the correction of technical complication.
Thrombolytic therapy is usually the treatment of choice in the late transplant period.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively . Conclusions:
1) Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures.
2) A meticulous postoperative protocol is critical to graft and patient survival.
3) A coordinated multidisciplinary team approach is crucial in improving successful outcomes regarding such complex and urgent situations.
4) The prevention of TRVT, is always more effective than treatment .
Q2- What is the level of evidence provided by this article?
Level of evidence is 5.
Dalia Ali
2 years ago
Transplant renal vein thrombosis usually occurs early after surgery with a reported prevalence of 0.1% to 4.2%. It is a devastating event that ultimately leads to graft loss in almost all cases. There are many pre disposing factors related to donor, recipient, surgery, and immunosuppression, with mechanical factors being considered the most common causes of transplant renal vein thrombosis.
Transplant renal vein thrombosis (TRVT) of an
allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants. Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.
Causes of transplant renal vein thrombosis The pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression. When considering donor risk factors, use of a
donor’s right kidney is associated with the devel opment of renal graft thrombosis
Recipient-related risk factors include extremes of
age,which may call for more complex sur gical procedures, especially with atherosclerotic vessels predisposing to a higher incidence of thrombosis, and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures. Other recipient-related risk factors include pretransplant dialysis modality,in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene. Perioperative hemodynamic status, in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis, and primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
Clinical diagnosis may be easy in cases of acute
renal vein thrombosis, although not specific, with diagnosis perhaps confused with the occurrence of a urologic complication or acute rejection, the 2 most frequent complications during the early post operative period. Transplant renal vein thrombosis may be complicated by pulmonary embolism, especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins
Diagnosis of transplant renal vein thrombosis The diagnosis of TRVT is usually based on a highly suspicious clinical presentation, triggering assess ment using duplex ultrasonography. The clinical diagnosis can be difficult in cases of chronic vein thrombosis, as it is initially asymptomatic. Conventional gray-scale ultrasonography with
color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and long-term outcomes of noncomplicated renal transplants
Duplex ultrasonography characteristically reveals
reversed arterial diastolic flow (ie, the arterial wave form positive during systole and negative during diastole), a spike-like systolic component, and nonvis ualization of the renal vein. Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels.This high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss
The reversed diastolic waveform was described
(in the main or segmental renal arteries), when retrograde blood flow occurred at any time point during the diastole, regardless of whether antegrade flow has happened.
Magnetic resonance imaging is now considered a
reliable tool for evaluation of renal allografts and the diagnoses of most complications. Magnetic reso nance angiography is increasingly used to screen for vascular abnormalities in renal allografts . Due to fear of nephrogenic systemic fibrosis after gadolinium-based contrast agents in patients with decreased glomerular filtration rate, imaging modalities have been developed to view the vessels without intravenous contrast.
Management of transplant renal vein thrombosis Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical manage ment of vascular complications must include surgical exploration of the allograft. Successful emergency surgical thrombectomy has
been reported in the early posttransplant period. Operative interventions can facilitate better evalu ation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis
Combined percutaneous mechanical thrombec tomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT, notably after the second week after transplant with subacute or chronic TRVT and also in acute TRVT when prolonged thrombolysis has failed or is contraindicated.
Preventive strategies Because graft thrombosis is difficult to treat and graft loss is the usual outcome, development of preventive strategies is of paramount importance. First, tech nical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable impor tance in avoidance of TRVT.
Attention to intravascular volume status in pa tients undergoing renal transplant is recom mended. Transesophageal Doppler has been used to monitor the fluid balance during the procedure because it has been more accurate than measurement of central venous pressure. Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention may result in successful salvage of a renal allograft
Conclusions
Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures. A meticulous postoperative protocol is critical to graft and patient survival. A coordinated multidisciplinary team approach is crucial in improving successful outcomes regarding such complex and urgent situations. The prevention of TRVT by careful attention to predisposing factors, including technical details of surgery procedures, is always more effective than treatment of this dreadful com plication, since it may be too late to salvage a renal allograft once TRVT has been established.
Last edited 2 years ago by Dalia Ali
Mu'taz Saleh
2 years ago
Introduction
Post transplant vascular complication is one of most important challenges , have a prevalence of 1% to 10% and including transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas
Transplant renal vein thrombosis (TRVT) is one of the main causes of early graft dysfunction after renal transplant, with prevalence of 0.1% to 4.2 % .
Causes of transplant renal vein thrombosis :
donor risk factors
Right donor nephrectomy
Multiple graft vessels
prolonged ischemia time
Older age of donors
Recipient-related risk factors
extreme age
pretransplant dialysis modality : peritoneal dialysis is associated with more graft thrombosis than hemodialysis
Pre transplant hypercoagulable status
Perioperative hemodynamic status : hypotension , dehydration .
Primary renal disease such as membranous nephropathy
technical risk factors
kinking of the graft vein,
long vein,
wide disparities in vessel size,
injury to the vascular endothelium
mechanical causes
kink in the renal vein,
compression by hematomas or lymphoceles,
anastomotic stenosis,
extension of an underlyingdeep venous thrombosis
immunosuppression risk factors
cyclosporine,
OKT3 antibody
high doses of pulsed methyl prednisolone, and anti -thymocyte/antilymphocyte globulin
Clinical manifestations of transplant renal vein thrombosis
rapid onset of oliguria or anuria
haematuria with worsening graft function
a painful swollen graft, which may progress to rupture,
haemorrhage and shock.
Chronic vein thrombosis is usually asymptomatic- thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Diagnosis:
Duplex ultrasonography: Used early post transplant to detect early complications, calculate resistive index and pulsatile index. Safe, noninvasive with no exposure to radiation or contrast media. Reveals reversed arterial diastolic flow, spike like systolic component and non visualization of renal vein, with 3 typical shapes of reversed diastolic waveforms, “transient”, “plateau” and “inverted M”. Isolated reversed or absent diastolic arterial flow is sensitive but not pathognomonic to TRVT. Diagnosis is affected by patient’s body habitus, operator skills and availability of acoustic window.
CT angiography: Provide definite diagnosis but invasive, use nephrotoxic contrast
Nuclear medicine scintigraphy and MR angiography: More sensitive than U/S, no nephrotoxic agents used. MR angiography with recent modalities used without contrast and screen for vascular complications. limited use due to higher cost, long examination time and lack portability.
Treatment of TRVT There are two treatment options for renal allograft venous thrombosis: thrombolytic therapy and surgical thrombectomy. Surgical examination of the allograft is required in the therapy of vascular problems. Thrombolytic therapy is typically the treatment of choice for late-stage TRVT. Combined percutaneous mechanical thrombectomy and catheter-directed thrombolysis have been tried safely and efficiently in TRVT, particularly after the second week following transplant with subacute or chronic TRVT, as well as in acute TRVT when extended thrombolysis has failed or is contraindicated. Prevention Because it may be too late to salvage a kidney transplant after TRVT has formed, prevention of TRVT by paying attention to predisposing variables, such as technical aspects of the surgery, is always more effective than treatment
What is the level of evidence provided by this article? 5
Mohammed Sobair
2 years ago
Introduction:
Postoperative vascular complications are major challenges, occurring in 1% to 10% of
transplanted patients.
The most common vascular complications:
Transplant renal artery stenosis.
Renal graft arterial or venous thrombosis.
Arterial injury:
Including arteriovenous fistulas, intrarenal pseudo aneurysms, arterial dissection, and
arterial-calyceal fistulas.
TRVT:
Prevalence of 0.1% to 4.2 % of all transplants. The prevalence of TRVT is higher in
deceased-donor than in living donor transplant.
Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all
cases.
Causes of transplant renal vein thrombosis:
Donor risk factors:
A donor’s right kidney.
Multiple graft vessels.
Prolonged ischemia.
Vascular injury.
Older age of donors.
Recipient-related risk factors:
Include extremes of age.
Pretransplant dialysis modality, in which peritoneal dialysis is associated with more
graft thrombosis than hemodialysis.
Perioperative hemodynamic status:
Hypotension and dehydration could predispose to acute kidney injury, hypo perfusion,
and thrombosis.
Primary renal disease such:
As membranous nephropathy.
Technical issues:
Including kinking of the graft vein, a long vein, wide disparities in vessel size, and injury
to the vascular endothelium during surgical manipulation.
Mechanical causes:
Are considered the most common causes of TRVT:
A kink in the renal vein, compression by hematomas or lymphoceles, anastomotic
stenosis, and extension of an underlying deep venous thrombosis.
Compression of the renal vein by the renal artery is another risk factor.
Immunosuppression:
Administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses
of pulsed methyl prednisolone, and anti – thymocyte/antilymphocyte globulin AND
Cyclosporine.
Clinical manifestations:
Rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful
swollen graft, which may progress to rupture, hemorrhage, and shock.
Chronic vein thrombosis is usually asymptomatic.
However, thrombocytopenia may occur.
Pulmonary embolism, especially when it is associated with and related to the extension
of deep vein thrombosis.
Diagnosis of transplant renal vein thrombosis:
The diagnosis of TRVT is usually based on a highly CLNICAL suspicious.
the arterial wave – form positive during systole and negative during diastole), a spike-like
systolic component, and nonvisualization of the renal vein.
Although angiography remains the criterion standard for the diagnosis of renal vascular
pathology, it is invasive and associated with significant nephrotoxicity.
Other investigations, such as nuclear medicine scintigraphy or magnetic resonance
angiography, offer excellent alternatives to the criterion standard with no nephrotoxicity
and a greater sensitivity than ultrasonography.
Management of transplant renal vein thrombosis:
Two strategies are available for treating venous thrombosis of renal allograft:
thrombolytic therapy and surgical thrombectomy.
Successful emergency surgical thrombectomy has been reported in the early
posttransplant period. Operative interventions can facilitate better evaluation of the
cause of thrombosis and can allow for the correction of technical complications.
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late
transplant period.
Combined percutaneous mechanical thrombectomy and localized catheter-directed
thrombolysis.
What is the level of evidence provided by this article?
level of evidence V.
Asmaa Khudhur
2 years ago
TRVT
Vascular complications Occurs in 1%to 10% of transplant patients.
Include:
1-Transplant renal artery stenosis
2-Renal arterial or venous thrombosis
3-Arterial injury including AV fistulas , intrarenal pseudo aneurysms, arterial dissection and arterial -calyceal fistulas.
TRVT is one of the main causes of DGF with prevalence of 0.1%_4.2% of all transplants.
Causes :
Multifactorials and include
Donor factors:
Use of Donor right kidney
Multiple graft vessels
Prolonged ischemia time
Vascular injury
Older age donor
Recipient factors:
Extremes of age
Pre transplant dialysis modality, more in PD
Perioperative hemodynamic status
Primary renal disease
Technical issues:
Kinking in graft vein
Long vein
Wide disparities in vessels size
Injury to vascular endothelium
Compression by hematoma or lymphocele
Anastomoses stenosis
Contra lateral transplant procedure
IS factors :
Cyclosporin , OKT3 antibody , high dose of methyl prednisolone and antithymocyte globuline.
Clinical manifestations:
Rapid onset of oliguria or anuria, hematuria with worsening graft function, painful swellen graft which may progress to rupture, hemorrhage and shock.
Chronic vein thrombosis is asymptomatic.
Diagnosis of TRVT:
Is based on highly suspicious clinical presentation.
Conventional gray-scale US with color and Doppler
Finding of isolated reversed or absent diastolic arterial flow is sensitive but not pathognmonic and non specific to TRVT . Acute rejection and ATN also present with reversed diastolic flow.
Angiography remain the criterion standard but it invasive with Nephrotoxicity.
MRI is considered reliable tool for evaluation of renal allograft and most complications.
Management of TRVT:
Thrombolytic therapy
Surgical thromboectomy
Level of evidence:5
Wael Jebur
2 years ago
Allograft vein thrombosis TRVT:
Allograft vein thrombosis is dreadful encounter in the context of kidney transplantation. Its taking place early post operatively. Multiple factors are interplaying, related to donor, recipient, medication and operative procedure itself.
Incidence: 1-4.2%.
Its resultant in allograft loss and nephrectomy in almost all cases. Donors Risk factors for ARVT:
1) Harvesting right kidney. Because of long artery and short vein thereof.
The short vein is increasingly vulnerable for consequent compression by swollen allograft secondary to ATN, Ischemic and rejection sequela.
Right kidney is increasingly difficult to implant than the left one due to possible multiple renal arteries, and long artery could be kinked.
prolonged cold ischemia time and vascular injury are reported to potentiate risk of venous thrombosis.
Old aged donors , due to hypotension and reperfusion injury facilitate procoagulant status on atherosclerotic. Recipients Risk factors for ARVT:
Extreme of age is a prominent risk factor attributed to size difference and atherosclerotic changes.
Interestingly peritoneal dialysis is more prone for ARVT than hemodialysis patients.
Peri-operative hypotension and dehydration might cause AKI ATN , hypo-perfusion and thrombosis .
Membranous nephropathy is linked to higher incidence.
Surgical procedure related risk factors:
long vein is a risk factor for kinking ,
injury to endothelium during manipulation.
Compression by lymphocele and hematoma.
Contralateral transplantation is another risk factor owing to compression by renal artery.
Medications related risk factors for TRVT:
CNi are associated with thrombosis attributed to its thrombogenic tendency , as its increasing liberation of thromboxane A2, thromboplastin, factor VIII platelets aggregability and reduced thrombomodulin.
Presentation:
Acute anuria and oliguric with allograft pain and tenderness with progressive swelling that might progress to rupture and shock .
chronic thrombosis is asymptomatic. Thrombocytopenia might be prominent sign.
pulmonary thromboembolism Differential Diagnosis:
Acute rejection Diagnosis:
gray-scale US
Duplex US.
MRI is the best recommended investigation due to limitation of the first 2 modalities.
Preventive measures are best treatment to avoid catastrophic complication of TRVT.
Manal Malik
2 years ago
Summary of Transplant Renal Vein ThrombosisIntroduction
Postoperative surgical complication of kidney transplanted patient from 1% to 10%.
Transplant renal vein thrombosis is one of the main causes of early graft dysfunction.
After renal transplant is about 0.1 to 4.2% of all transplants.
Usually RVYT events lead to graft loss and nephrectomy in almost cases. Causes: 1- Donor factors:
Use donor’s right kidney due to short vein and long artery.
Multiple graft vessels.
Prolong ischemia time.
Vascular injury.
Older age of donor. 2-Recipient -related risk factors:
Extreme age.
Variation in vessels size between the donor and recipient .
Mode of renal replacement therapy more in PD dialysis.
hypercoagulable states.
perioperative haemodynamic status.
primary renal disease like membranous nephropathy.
3-mechnical causes which is common are:
akink in the renal vein .
Compression by hematoma or lymphocele .
anastomotic stenosis.
Extension of an underling deep venous thrombosis.
Compression of renal vein by renal artery especially in contralateral transplant procedure.
Immunosuppression TRVT can be triggered by administration of prothrombotic medication.
Such as cyclosporine CKT3 antibody .high dose of pulse methylprednisolone ,ATG. Clinical manifestation of RVT:
1- Rapid onset of oliguria or anuria.
2- Haematuria.
3- Worsing graft function.
4- Painful swollen graft.
may progress to rupture haemorrhaged and shock. Chronic vein thrombosis:
1-asymptomtic
2- thrombocytopenia. Occur in few hours. Diagnosis of transplant renal vein thrombosis.
Based on highly subspinous clinical presentation.
Duplex u/s
As vascular anastomosis are deep in the recipient pelvis ,thrombus in the renal vein is rarely seen an conventual ultrasound imaging.
Duplex ultrasonography reveals arterial diastolic flow.
Spike -like systolic complement and non visualization of renal vein .
Reversed or absent diastolic flow is assign of extremely high vascular resistance in small interareal artery or large extrarenal vessels .
The high vascular resistance indicate graft dysfunction.
Increased the risk of graft loss.
There are 3 typical shape of reversed diastolic waveform:
1- Type 1 or transient waveform seen in sever rejection or acute tubular necrosis of the graft
2- MRI used to screen vascular abnormalities in renal allograft without i.v contrast but not suitable functional ill patients Management of transplant renal vein thrombosis:
Two treatment are available for treating venous thrombosis:
1-thrombolytic therapy .
2-surgical thrombectomy.
Successful emergency surgical thrombectomy which is include surgical exploration of the allograft .
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period .
Combined percutaneous mechanical thrombectomy and localized catheter.
Directed thrombolysis is effectively in TRVT. Prevention strategies:
Sufficient training in the techniques of vascular anastomosis and graft recovery is critical
Avoid long renal vein transplant kidney
Preferable ipsilateral transplant when ever possible.
Use transoesophageal doppler to monitor the fluid balance during the procedure because it has been more accurate. Conclusion
High risk patients should be followed postoperatively to allow proper diagnosis and prophylactic measures:
Multidisciplinary team approach is crucial in improving successful outcomes such as complex and urgent situation . Prevent TRVT measurementIncluding technical surgical procedures details.
level evidence 5
.
CARLOS TADEU LEONIDIO
2 years ago
Please summarise this article
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants. Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.The prevalence of TRVT is higher in deceased-donor than in living-donor transplant. CAUSES OF TRANSPLANT RENAL VEIN THROMBOSIS The pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression. Donor risk factors: – use of a donor’s right kidney – Multiple graft vessels – Older age of donos Recipient-related risk factors – extremes of age – pretransplant dialysis modality in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, Mechanical causes – a kink in the renal vein – compression by hematomas or lymphoceles – anastomotic stenosis – extension of an underlying deep venous thrombosis Prothrombotic drugs – cyclosporine; – OKT3 antibody, – high doses of pulsed methyl prednisolone; – anti – thymocyte/antilymphocyte globulin CLINICAL MANIFESTATIONS
The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and Shock. Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
DIAGNOSIS
Conventional gray-scale ultrasonography with color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and long-term outcomes of noncomplicated renal transplants
MANAGEMENT
Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical management of vascular complications must include surgical exploration of the allograft.
Successful emergency surgical thrombectomy has been reported in the early posttransplant period. Operative interventions can facilitate better evaluation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.
Thrombolytic therapy is usually the treatment of choice occurring in the late transplant period. Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state, but thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated
What is the level of evidence provided by this article?
Level 05 – narrative review
rindhabibgmail-com
2 years ago
Allograft vein thrombosis is bit rare complication of transplantation affecting around 2 to 4%. Risk factor could be prolonged ischemia time, old age, right sided donor kidney, perioperative hypotension, kinking of graft vein, raff vascular handling and injury. Usually these patient present with anuria, worsening graft function.
Can be treated with thrombectomy and thrombolysis.
Level V
Hinda Hassan
2 years ago
1. Please summarise this article
Transplant renal vein thrombosis is a serious complication that can end with graft loss. Many risk facors can lead to this and they include: use of a donor’s right kidney, multiple graft vessels, prolonged ischemia, older age of donors, Recipient extremes of age, variations in vessel sizes between the donor and recipient, pretransplant dialysis modality , hypercoagulable states, prothrombotic drugs (such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti thymocyte/antilymphocyte globulin), perioperative hemodynamic status, primary renal disease, kinking of the graft vein, a long vein, wide disparities in vessel size, injury to the vascular endothelium during surgical manipulation, renal veincompression by hematomas or lymphoceles, anastomotic stenosis, extension of an underlying deep venous thrombosis and compression of the renal vein by the renal artery.
Clinical manifestations include rapid onset oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock. On the other hand, chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Diagnosis is usually clinical and through use of duplex ultrasonography. The gold standard method is angiography but it is invasive and is associated with nephrotoxicity. Nuclear medicine scintigraphy or MRA are other alternative diagnostic tools.
Management involves thrombolytic therapy , surgical thrombectomy and combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis . 1. What is the level of evidence provided by this article?
Level V
MICHAEL Farag
2 years ago
What is the level of evidence provided by this article? Level V
Causes of transplant renal vein thrombosis donor risk factors:
– use of a donor’s right kidney is associated with the development of renal graft thrombosis due to the short vein and long artery of the right kidney – Multiple graft vessels have been also implicated in renal graft thrombosis – prolonged ischemic time
– vascular injuries
– Older age of donors is associated with an in – creased risk of graft thrombosis Recipient-related risk factors
– extremes of age which may call for more complex surgical procedures, especially with atherosclerotic vessels – pretransplant dialysis modality in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable state – Perioperative hemodynamic status,11,26 in which hypotension and dehydration could predispose to thrombosis – Regarding immunosuppression, TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody
Huda Saadeddin
2 years ago
The diagnosis of transplant renal vein thrombosis depends on a high index of clinical suspicion and duplex ultrasonographic scans.
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants.
Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.
When considering donor risk factors, use of a donor’s right kidney is associated with the development of renal graft thrombosis.
prolonged ischemia time and vascular injuries have been found to be donor risk factors for renal graft thrombosis.
Older age of donors is associated with an increased risk of graft thrombosis.
Other recipient-related risk factors include pretransplant dialysis modality, in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis.
The following mechanical causes are considered the most common causes of TRVT: a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
Regarding immunosuppression, TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and antithymocyte/antilymphocyte globulin
Clinical manifestations of transplant renal vein thrombosis
The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial waveform positive during systole and negative during diastole), a spike-like systolic component, and nonvisualization of the renal vein
Successful emergency surgical thrombectomy has been reported in the early posttransplant period. Operative interventions can facilitate better evaluation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.11,55,56
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period. 57-60 Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state, 54 but thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated.55,61 However, this is not the case in every patient; there are reports of successful thrombolytic therapy in the early posttransplant period.54
Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures. A meticulous postoperative protocol is critical to graft and patient survival. A coordinated multidisciplinary team approach is crucial in improving successful outcomes regarding such complex and urgent situations. The prevention of TRVT by careful attention to predisposing factors, including technical details of surgery procedures, is always more effective than treatment of this dreadful complication, since it may be too late to salvage a renal allograft once TRVT has been established.
level V
Farah Roujouleh
2 years ago
Transplant renal vein thrombosis usually occurs early after surgery with a reported prevalence of 0.1% to 4.2%.
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant
The prevalence of TRVT is higher in deceased-donor than in livingdonor transplant Causes of transplant renal vein thrombosis Donor factors right kidney , Multiple graft vessels , Prolonged ischemia time , Vascular injury
Old age Recipient factorsn old age , Pretransplant dialysis modality , Perioperative hemodynamic status
Primary renal disease Mechanical factors Kinking of graft vein, compression , Long vein , Wide disparities in vessel size
Injury to the vessels during surgical manipulation Immunosuppression medx Cyclosporin , High doses of methylpred , ATG Clinical manifestation
Rapid onset of oliguria or anuria, hematuria , worsening graft function,
thrombocytopenia Complications :pulmonary embolism and DVT Diagnosis:
– duplex Ultrasonography
It can reveal reversed arterial diastolic flow (arterial wave form positive during systole and negative during diastole)
Reversed diastolic flow is a sign of extremely high vascular resistance.
– Angiography :Invasive and carry a risk of nephropathy
-Nuclear medicine scintigraphy
-MRA Management
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant
period. can cause life-threatening hemorrhage
Surgical thrombectomy has risks associated with anesthesia and postoperative infection
in an immunosuppressed state,
Combined percutaneous mechanical thrombectomy and localized catheter directed thrombolysis: safe and effective
level of evidence 5
Balaji Kirushnan
2 years ago
Transplant renal vein thrombosis: (TRVT)
This complication occurs in the early post operative phase usually within 4 weeks of surgery… The incidence of this devastating complication is 0.1-4.2% …. It is one of the main complications after surgery leading to acute graft dysfunction and graft nephrectomy in the major of the cases… It also is a clinical masquerader to urine leak, urinoma and lymphocele…
Causes of TRVT: The causes of TRVT include a multifactorial approach namely
Donor factors: It is more common in deceased donor transplants as the ischemia time and the chance of endothelium damage is more in these patients. It is more common in donors with longer ischemia time and those with multiple renal arteries…Many reports have indicated that renal vein thrombosis is due to right kidney selection where there is short renal vein and long artery.. the right kidney due to long artery can get compressed if there is acute graft dysfunction due to any other causes.. Old age of the donors are associated with increased thrombogenicity….Delayed Graft function in the old age can be associated with hypotension and ischemia reperfusion injury can aggravate cytokine release and endothelium damage ..
Recipient factors: extremes of age with atherosclerotic vessels are a risk factor as it may lead to thrombosis after a small intimal injury… discrepancies between the donor and recipient kidneys i.e pediatric recipient receiving an adult kidney….Other recipient factors include primary renal disease like membranous nephropathy, APLA syndrome are known to be associated with TRVT…The modality of the dialysis before transplant has a strong influence on the development of TRVT… Peritoneal dialysis has a higher incidence of TRVT due to elevated levels of procoagulant levels in the blood and hypercoagulable states ..Pre operative hemodynamic status of the recipient with hypotension and dehydration can pre dispose to RVT..
Variety of technical factors have been implicated in RVT: short artery, kinking of the vein if too long, external compression from the lymphocele or urinoma or seroma…. RVT is more common in contra lateral setting i.e left kidney for the right side and the right kidney for the left side.. Other causes include disparity in the renal arteries and vein in pediatric and adult kidney.. Injury to the vascular endothelium during manipulation has also been described to cause RVT.
Immunosuppression: regarding the incidence of RVT after the use of Prothrombotic drugs like Cyclosporine, OKT3 antibody, high dose of steroids and ATG. cyclosporine can cause enhanced platelet aggregation, enhancement of thromboxane A2 and decreased thrombomodulin activity…
clinical signs:
Sudden onset of graft pain and tenderness with oliguria and hematuria is described as the classical signs of TRVT. If not identified it may progress to shock and graft rupture..chronic renal vein thrombosis maybe asymptomatic…Sometimes clinical diagnosis maybe skewed when TRVT is associated with acute rejection or lymphocele.. One should always be vigilant for the development of pulmonary embolism..
Diagnosis:
Ultrasound may show decreased echoes of the kidneys due to edema of the kidney…Duplex ultrasound has been shown to be diagnostic of the condition…It shows reversed arterial diastolic flow (positive during systole and negative during diastole) and spike like systolic component. .There are 3 types of reversed diastolic flow in the graft//Transient reversal/ Plateau type/ M type reversal…Absent of reversed diastolic flow is sensitive but not specific for the TRVT. It can be seen in advanced graft rejection, severe ATN, or severe compression or kink by the any external collection…visualization of the thrombus by USG doppler is challenging as it may be deep
CT angiography can diagnose the condition but it required exposure to contrast with risk of graft injury…..MR angiography is non nephrotoxic and can pick up RVT. Scintigraphy studies also known to identify the condition….
Surgical treatment of RVT involves graft thrombectomy either catheter directed or mechanical means of catheter directed, but these procedures are not associated with success…
Medically patients must be on IV heparin and long term anticoagulation is indicated…serial repeated doppler can tell if the RVT is resolving….
Unfourtunate cases of graft nephrectomy have been done after extensive TRVT.. Preventive techniques by enhancing surgical enterprise and low dose aspirin with LMWH have been implicated to prevent TRVT in high risk cases like multiple vessels
this is a review article is level 5 ..review article or expert opinion
Sahar elkharraz
2 years ago
Renal vein thrombosis
It’s a common problem post transplant.
It’s account 1 to 10% transplant patients.
Other common vascular complications post transplant are,
transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
Renal vein thrombosis is the main cause of early graft dysfunction and graft loss and nephrectomy.
There’s many causes of renal vein thrombosis related to donor and recipient and technical issues.
Donor causes:
Right kidney associated with renal vein thrombosis because of short vein and long artery.
Multiple vessels of graft predispose graft to vascular injury and acute tubular necrosis and urine obstruction.
Older donor also lead to renal vein thrombosis.
variations in vessel sizes between the donor and recipient.
Extreme age of recipient and hemodynamic instability like hypotension and dehydration.
Pretransplant dialysis modalities because peritoneal dialysis more prone to renal vein thrombosis more than haemodialysis.
primary renal disease like membranous nephropathy.
Technical issues like kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
Immunosuppressive therapy like cyclosporine induced renal vein thrombosis post transplant.
Clinical manifestations of transplant renal vein
thrombosis.
Anuric or oliguria with hematuria and rapid deterioration of graft function and severe graft pain.
It’s may complicated to pulmonary embolism.
Diagnosis by duplex ultrasonography.
it’s safe and noninvasive shows plateau like or inverted M waveform.
Renal angiography is diagnostic but invasive and nephrotoxic.
Other helpful in diagnosis and less nephrotoxic nuclear medicine scintigraphy or magnetic resonance angiography.
Magnetic resonance imaging but limited in patients with low eGFR because gadolinium toxicity and also limited in patients with pacemaker.
Treatment of renal vein thrombosis:
Anti thrombolytic therapy and surgical thrombectomy but thrmolytic therapy carries risk of bleeding.
Combined percutaneous mechanical thrombec- tomy and localized catheter directed thrombolysis is used now safely.
Prevention of renal vein thrombosis:
Good training for vascular anastomoses of renal vessels during operation to avoid vessel injury and damage or kink.
routinely shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
Good assessment of volume status and good hydration
Dail assess urine output and creatinine level and electrolytes.
Daily doppler ultrasound post transplant in first weeks for timely diagnosis.
Low dose aspirin and low molecular weight heparin especially in patients with hypercoagulablity status.
What is the level of evidence provided by this article? Level 5
Amna Khalifa
2 years ago
Transplant renal vein thrombosis
Post operative vascular complications considered major challenge during renal transplant surgery, occurs 1-10% of the kidney transplant.
1. These complications includes renal artery stenosis
2. Renal allograft arterial or venous thrombosis
3. Arterial injury such are
· arterial AV fistulae,
· intrarenal aneurysm,
· arterial dissection,
· arterial -calyceal fistulas.
Causes of transplant RVT
1. Donor factors
· Donors rt kidney (short vein, long artery)
· Multiple graft vessels
· Prolonged ischemia
· Vascular injury
· Old age of donors (hypotension, ischemic reperfusion)
2. Recipient factors
· Extremes of age (elderly -atherosclerotic vessels, pediatric with variation in vessel sizes between the donor and recipient).
· Pretransplant dialysis modality (PD associated with RVT due to high procoagulant factor, hypercoagulable state)
· Perioperative hemodynamic status (hypotension, dehydration).
· Primary renal disease such as membranous GN
3. Technical factors
Kinking of graft vein, compression by hematoma /lymphocele/anastmotic stenosis
Long vein
Wide disparities in vessel size
Injury to the vascular endothelium during surgical manipulation
Compression of the renal vein by the renal artery esp. in the contralateral transplant procedure (rt kidney in lt iliac fossa)
4. Immunosuppressant
Prothrombotic drugs such as
Cyclosporin
OKT3 antibody
High doses of pulse steroid
ATG
Clinical manifestation of transplant RVT
Rapid onset of oliguria or anuria, hematuria , worsening graft function, painful swollen graft prone for rupture or hemorrhage.
In chronic RVT thrombocytopenia as a consequence of platelets sequestration.
The clinical presentation can be confused with urological complications.
Diagnosis:
Depends on highly suspicious clinical presentation Requires duplex Ultrasonography
(conventional gray scale ultrasonography with color and spectral doppler, with calculation of resistive index and pulsatile index)
It can reveal reversed arterial diastolic flow (arterial wave form positive during systole and negative during diastole)
Reversed diastolic flow is a sign of extremely high vascular resistance.
Angiography :Invasive and carry a risk of nephropathy Other considered excellent alternative with no nephrotoxicity Nuclear medicine scintigraphy MRA
MRI is also reliable tool however there is a fear of nephrogenic systemic fibrosis. Its limitations include greater cost lack of portability and prolong examination time also cant be used in patients with pacemakers.
Management of transplant RVT
· Thrombolytic therapy: treatment of choice for transplant RVT however it can be associated with life threatening hemorrhage/ clot migration.
· Surgical thrombectomy: has risk of anesthesia, post operative infection
· Combined percutaneous mechanical thrombectomy and localized catheter directed thrombolysis: safe and effective
Preventive strategies:
5. Sufficient training
6. Avoid long renal vein
7. To do Ipsilateral transplant
8. Attention to intravascular volume
9. Use of ultrasound foe early monitoring
10. To use postoperative protocols to monitor for
· Hrly urine output
· Daily duplex uss
· Daily serum creatinine and electrolytes
· Low dose aspirin
· Low molecular weight heparin
level of evidence 5
Zahid Nabi
2 years ago
Transplant renal vein thrombosis is a rare complication of kidney transplant affecting 1 to 4.2% of patients. Risk factors are Donor driven Right sided donor kidney having short renal vein. Prolonged ischemia time. Old age of donor.
Recipient related risk factors include Extremes of age. Peritoneal dialysis Perioperative hypotension and dehydration.
Technical Risk factors kinking of graft vein Long vein Injury to vascular endothelium during surgical manipulation. Compression of renal vein by renal artery is another risk factor especially in contra lateral transplant procedures. Amongst immunosuppression Cyclosporine can increase the risk
CLINICAL MANIFESTATIONS Oliguria or anuria Hematuria with worsening graft function chronic renal vein thrombosis is usually asymptomatic.
DIAGNOSIS OF RVT Color Doppler ultrasound is easily available and non invasive way of diagnosis. Reversed diastolic flow is suggestive though it can also be seen in ATN, acute rejection, hematoma and vascular Leak. CT angio Renal scan MRI are other means of diagnosis each having its own pros and cons.
MANAGEMENT The key point in management is early diagnosis Thrombolytic therapy is usually treatment of choice Surgical exploration and thrombectomy is another alternative. Combined percutaneous mechanical thrombectomy and Localized catheter directed thrombolysis have been tried safely and effectively.
CONCLUSION High risk patients should be identified. Meticuolous post transplant protocol should be adopted for early diagnosis and intervention. A coordinated multidisciplinary approach is needed to manage such patients.
Yashu Saini
2 years ago
INTRODUCTION
Transplant vein thrombosis is a catastrophic event in terms of long term graft survival. It causes graft loss in almost all cases.
Prevalence of the disease is usually 0.1 to 4.2 %. there are number of post operative vascular complications in transplanted patients. The most common are:
Transplant renal artery stenosis
Renal vein thrombosis
A-v fistula
Intrarenal pseudoaneurysms
Arterial dissection
Atrerial-Calyceal fistula
CAUSES OF TRANSPLANT RVT
DONOR FACTORS
Donor’s right kidney
Multiple graft vessels
Prolonged ischemia time
Vascular injuries
Older donor age
RECIPIENT RISK FACTORS
Extremes of age
variation of vessal size between donor and recipient
hypotension
dehydration
MECHANICAL CAUSES
kink in renal vein
Compression by hematomas or lymphoceles
compression of renal vein by renal artery
IMMUNOSUPPRESSION – Cyclosporine
CLINICAL FEATURES
Rapid onset oliguria / anuria
Hematuria with worsening graft function
Painful swollen graft
Hemorrhage
Shock
Pulmonary embolism
Extension of DVT to lower limbs
DIAGNOSIS
Conventional ultrasonography with spectral doppler
Duplex ultrasonography is superior
MRI
MANAGEMENT
Thrombolytic therapy – Therapy of choice
Surgical thombectomy
patients who are at high risk of developing transplant vein thrombosis should be meticulously followed up post operatively sop that prompt diagnosis and necessary measures can be taken timely.
The prevention of TRVT by careful attention to predisposing factors, including technical details of surgery procedures, is always more effective than treatment of this dreadful complication.
amiri elaf
2 years ago
# Please summarise this article
* Transplant renal vein thrombosis usually occurs early after surgery with a reported prevalence of 0.1% to 4.2%. It is leads to graft loss in almost all cases.
# Causes of transplant renal vein thrombosis
The pathogenesis are multi-factorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
# The donor risk factors:
1 *Use of a donors right kidney is associated with the development of renal graft thrombosis( due to the short vein and long artery of the right kidney).
2*Multiple graft vessels
3*Prolonged ischemia
4*Older age of donors
# Recipient risk factors:
1*Extremes of age especially with atherosclerotic vessels and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures.
2*Peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
3*Hypotension and dehydration
# Technical factors
1*Kinking of the graft vein
2*Long vein
3*Wide disparities in vessel size
4*Injury to the vascular endothelium during surgical
manipulation.
*The following mechanical causes are considered the most common causes of TRVT:
* Kink in the renal vein,
* Compression by hematomas or lymphoceles,
* Anastomotic stenosis
*Extension of an underlying DVT
*Compression of the renal vein by the renal artery is another risk factor, especially in contra-lateral transplant procedures
# Regarding immunosuppression factor:
*TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and ATG.
#Clinical manifestations of TRVT
*Rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
*Chronic vein thrombosis is usually asymptomatic, but thrombocytopenia may occur after a few hours
# Clinical diagnosis
*The diagnosis of TRVT is usually based on a highly suspicious clinical presentation,
*Duplex ultrasonography.
*Nuclear medicine scintigraphy or magnetic resonance angiography, offer excellent alternatives to the criterion standard with no nephrotoxicity and a
greater sensitivity than ultrasonography.
*Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
#Management of TRVT
*Two strategies are available:
A* Thrombolytic therapy: is usually the treatment of choice for TRVT occurring in the late transplant period.
B*Surgical thrombectomy: successful emergency surgical thrombectomy has
been reported in the early post-transplant period.
* Operative interventions can facilitate better evaluation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.
C*Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT
# Conclusions
*Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures.
* A meticulous postoperative protocol is critical to graft and patient survival.
*A coordinated MDT approach is crucial
* The prevention of TRVT by careful attention to predisposing factor, including technical details of surgery procedures.
# What is the level of evidence provided by this article?
*Level 5
Weam Elnazer
2 years ago
Introduction:
Transplant renal vein thrombosis (TRVT) is one of the leading causes of early graft malfunction following renal transplant, affecting 0.1% to 4.2% of all transplants. Transplant renal vein thrombosis nearly always causes graft loss and nephrectomy.
Risk Factors: -Related to the donor:
using Rt kidney, Multiple graft vessels, prolonged ischemia time, vascular injuries, and Older age.
-Related to the recipient:
extremes of age, pretransplant dialysis modality, in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, hypotension, dehydration, and primary renal disease such as membranous nephropathy.
-technical issues:
kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and DVT extension. The renal artery compressing the renal vein is another risk factor., for a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
Regarding immunosuppression:
cyclosporine, OKT3 antibody, high doses of pulsed methylprednisolone, and anti-thymocyte/anti-thymocyte globulin.
Transplant renal vein thrombosis symptoms:
Rapid onset oliguria or anuria, hematuria with worsening graft function, and a painful swelling graft may lead to rupture, bleeding, and shock.
Asymptomatic chronic vein thrombosis. Platelet sequestration in the thrombus may cause thrombocytopenia within a few hours.
Renal vein thrombosis diagnosis:
A worrisome clinical presentation triggers duplex ultrasonography to diagnose TRVT. Duplex ultrasonography shows reversed arterial diastolic flow, a spike-like systolic component, and non visualization of the renal vein.
Renal vein thrombosis management:
Thrombolytic treatment and surgical thrombectomy may treat renal allograft thrombosis. Vascular problems must be treated with allograft exploration.
-Prevention of TRVT by paying attention to predisposing variables, including technical specifics of the surgery, is always more successful than therapy, because it may be too late to salvage a kidney allograft once TRVT has developed.
Level of evidence V, narrative review.
Theepa Mariamutu
2 years ago
Transplant Renal Vein Thrombosis
devastating complication causing early graft dysfunction
prevalence of 0.1% to 4.2% of all transplants.
leads to graft loss and nephrectomy in almost all cases. It is more common in deceased donor than in living donor.
Causes
Donor factors:
Donor’s right kidney
due to short vein and long artery of the right kidney- can be easily compressed by kidney swelling due to ischemic damage, acute tubular necrosis, or urinary obstruction.
The kidney is more difficult to position especially if multiple renal arteries are present and the long renal artery can be easily kinked.
Multiple graft vessels
Prolonged ischemia time – potentiate thrombogenicity of the endothelium or cause ATN with graft oedema that led decreased perfusion and thrombosis.
Vascular injuries
Older age of the donor- donor hypotension and ischemia reperfusion injury which cause activation of the procoagulant surface from cytokines response and atherosclerotic vessels.
Recipient-related risk factors
Extreme of age especially with the atherosclerotic vessels
Variation in the vessels sizes between the donor and recipient, especially with paediatric transplantation.
Pretransplant dialysis modality; graft thrombosis is more in peritoneal dialysis than haemodialysis.
Hypercoagulable states; as antiphospholipid syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
Perioperative hemodynamic status: hypotension cause AKI, hypoperfusin and thrombosis.
Primary renal disease like membranous nephropathy.
Technical and mechanical issues
Kinking of the graft vein,
a long vein
wide disparities in vessel size
injury to the vascular endothelium during surgical manipulation
Compression of the vessel by hematoma, or lymphoceles or by renal artery in contralateral transplant procedure-right kidney into the left iliac fossa and left kidney into the right iliac fossa.
Anastomotic stenosis
Extension of an underlying DVT
Immunosuppressive drugs
Prothrombotic drugs such as cyclosporine, OKT3 antibody, high dose methylprednisolone, and anti –
thymocyte/antilymphocyte globulin.
Clinical manifestations of transplant renal vein thrombosis
rapid onset of oliguria or anuria
haematuria with worsening graft function
a painful swollen graft, which may progress to rupture,
haemorrhage and shock.
Chronic vein thrombosis is usually asymptomatic- thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Diagnosis of transplant renal vein thrombosis
Duplex ultrasonography, Conventional gray-scale ultrasonography with colour and spectral Doppler – early detection of complications and evaluation of the renal allograft- allows calculation of resistive index and pulsatile index
Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial wave-form positive during systole and negative during diastole), a spike-like systolic component, and nonvisualization of the renal vein.
There are 3 typical shapes of reversed diastolic waveforms:
type 1 or “transient” waveform, in which the reversed diastolic waveform returns to baseline before end diastole
type 2 or “plateau” waveform in which a flat reversed flow remains relatively constant throughout diastole
type 3 or “inverted M” waveform, in which reversed flow throughout diastole has mid-diastolic deceleration.
Angiography remains the golden standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
MRI is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
Management of transplant renal vein thrombosis
Thrombolytic therapy is usually the treatment of choice for late transplant period.
surgical thrombectomy in the early post-transplant period.
♧ Introduction
▪︎One of the most common vascular complications after renal transplantation is transplant renal vein thrombosis (TRVT) and it is
one of the main causes of early graft dysfunction, with a reported prevalence of 0.1% to 4.2 % of all transplants which is higher deceased-donor than in living donor. It’s events lead to graft loss and nephrectomy in almost all cases. ◇ Causes of transplant renal vein thrombosis ▪︎Includes: donor factors,
recipient factors, technical issues during transplant
surgery (operative factors), and immunosuppression. Donor- related risk factors:
1. Use of a donor’s right kidney (due to the short vein and long artery of the right kidney).
2. Multiple graft vessels
3. Prolonged ischemia time
4. Vascular injuries
5. Older age Recipient-related risk factors:
1. Extremes of age
2. Peritoneal dialysis
3. Perioperative hemodynamic status which cause acute kidney injury, hypoperfusion, and thrombosis
4. Primary renal disease such as membranous Technical issues:
1. Kinking of the graft vein or a long vein
2. Wide disparities in vessel size.
3. Injury to the vascular endothelium Mechanical causes:
1. Kink in the renal vein
2. Compression by hematomas or lymphoceles.
3. Anastomotic stenosis.
4. Extension of an underlying DVT.
5. Compression of the renal vein by the renal artery, especially in contralateral transplant procedures (right kidney into the left iliac fossa and left kidney into the right iliac fossa). Immunosuppression:
1. Administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and ATG. Clinical manifestations of transplant renal vein thrombosis
▪︎The typical clinical presentation is usually rapidonset of oliguria or anuria, hematuria with wor ▪︎Sening graft function, and a painful swollen graft,
which may progress to rupture, hemorrhage, and
shock.
▪︎Chronic vein thrombosis is usually asymp –
tomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet
sequestration in the thrombus. ◇ Differential diagnosis of acute TRVT,
1. Urologic complication.
2. Acute rejection Complication of TRVT: pulmonary embolism, Diagnosis of transplant renal vein thrombosis
1. Clinical diagnosis (can be difficult in cases of chronic vein thrombosis).
2. Duplex ultrasonography.
3. Conventional gray-scale ultrasonography with color and spectral Doppler
4. Angiography but it is invasive and associated with significant nephrotoxicity.
5. Nuclear medicine scintigraphy or MRA, offer excellent alternatives to the criterion standard with no nephrotoxicity and a
greater sensitivity than ultrasonography.
▪︎Limitations of magnetic resonance
i. Inability to image patients with pace makers,
ii. Greater cost
iii. Lack of portability.
iv. Prolonged examination time. Management of transplant renal vein thrombosis
Two strategies
1.Thrombolytic therapy
2. Surgical thrombectomy.
3. Combined percutaneous mechanical thrombec –
tomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT, notably after the second week after transplant with subacute or chronic TRVT and also in acute TRVT when prolonged thrombolysis has failed or is contraindicated. Preventive strategies
1. Sufficient training in the techniques of vascular anastomosis and graft recovery is critical.
2. Avoid multiple attempts during the operation.
3. Shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
4. Ipsilateral transplant whenever possible and also in cases of short renal vessels.
5.Attention to intravascular volume status
6. Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention.
7. Strict protocols for postoperative monitoring (an hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels.
8. Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients.
♧ Level of evidence: V
Huda Mazloum
2 years ago
● The most common vascular complications
** transplant renal artery stenosis
** renal graft arterial or venous thrombosis
** arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas
● Transplant renal vein thrombosis
** prevalence of 0.1% to 4.2 %
** lead to graft loss and nephrectomy in almost all cases
** The prevalence is higher in deceased-donor than in living-donor transplant.
This may be because living-donor
● Causes of transplant renal vein thrombosis:
** technical issues during transplant
** surgery (operative factors)
** donor’s right kidney
** Multiple graft vessels
** prolonged ischemia time
** Older age of donors
** Recipient extremes of age
** variations in vessel sizes between the donor and recipient
** pretransplant dialysis modality peritoneal dialysis is associated with more
graft thrombosis than hemodialysis
** elevated plasma procoagulant factors, hypercoagulable states,
** Perioperative hemodynamic status,
hypotension and dehydration could
** primary renal disease such as membranous nephropathy
** technical issues including kinking of the graft vein, a long vein wide disparities in
vessel size, and injury to the vascular endothelium
** contralateral transplant procedures
** drugs such as cyclosporine, OKT3 antibody, pulsed methyl prednisolone, and anti -thymocyte/antilymphocyte globulin
● Clinical manifestations :
** rapid onset of oliguria or anuria,
** hematuria
** worsening graft function
** a painful swollen graft,
** Chronic vein thrombosis is usually asymptomatic.
** thrombocytopenia after a few hours
Complications as urologic complication or acute rejection, pulmonary embolism,
● Diagnosis of TRVT is based on
** a highly suspicious clinical presentation,
** duplex ultrasonography with calculation of resistive index and pulsatile index,
** high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss
** Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
● Limitations of magnetic resonance imaging include
** inability to image patients with pace makers
** greater cost
** lack of portability
** prolonged examination time
● Management of transplant renal vein thrombosis
Two strategies are available :
** thrombolytic therapy
** surgical thrombectomy
● Thrombolytic therapy is usually the treatment of choice for TRVT in late period but thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated
● Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state
● Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT,
● Preventive strategies
** Sufficient training in the techniques of
vascular anastomosis
** A long renal vein is considered a risk factor of thrombosis
** ipsilateral transplant whenever possible
** Attention to intravascular volume status
** Transesophageal Doppler to monitor the fluid balance during the procedure
** clinical assessment and duplex ultrasonography monitoring during the
early posttransplant period
** Low-dose aspirin and low-molecular-weight heparin in high-risk patients
● Level 5
Marius Badal
2 years ago
SUMMARY:
INTRODUCTION:
One of the major challenges of kidney transplantation is post-operative vascular complications. The vascular complication can occur in about 1-10% of cases. They are:
1) Renal artery stenosis
2) Renal graft arterial or venous thrombosis
3) Intrarenal pseudoaneurysms
4) Arterial dissection and
5) Arterial calyceal fistulas
The article focuses on transplant renal vein thrombosis (TRVT) and which is one of the main causes of graft dysfunction after kidney transplantation. It can be occurring about 0.1-4.2% of all transplants.
The causes of TRVT are:
1) Donor related. Factors like prolonged ischemia time, older age, and multiple graft vessels can cause venous thrombosis
2) Recipient related. Factors like old age, antiphospholipid antibody, primary membranous nephropathy, and preoperative hemodynamic status.
3) Perioperative mechanical factors like hematoma that may cause compression, renal vein kinking, use of medications like ATG, cyclosporine, etc.
The diagnosis of TRVT:
1) The use of ultrasound and or duplex ultrasound
2) Venography/angiography
3) Medical scintigraphy
4) MRI
The management of TRVT:
Prevention of risk factors must be avoided or treated.
Starting of aspirin and or low molecular weight heparin
Thrombolytics and thrombectomy
Nephrectomy is the last resort if all fails
So in conclusion, preventing the risk factor is important. The cause needs to be treated. Once it has been diagnosed, treatment must be initiated like aspirin, and low molecular heparin to ensure to eliminate the thrombosis and to try to ensure the graft survives.
The level of the article is level 5
Radwa Ellisy
2 years ago
Renal vein thrombosis complicates 0.1-4.2% of renal tx operations.
It is a devastating complication and usually ends with graft nephrectomy.
Causes often multifactorial
– Donor related:
I. rt kidney donation: short vein could be compressed by swollen kidney
II. Prolonged ischemia increases the thermogenic ability of the endothelium
III. Multiple vessels is controversial
IV. Vascular injuries.
V. Older age.
– Recipient factors:
a. Older age and pediatric
b. Hypercoagulable state
c. PD more than HD
– Operation-related:
a. Renal vein kinking especially in contralateral tx
b. Compression by hematoma
– Immunosuppression:
CNI, high dose methylprednisolone and ATG
Clinical manifestation:
Acute: Oliguria or anuria, painful tender graft, graft dysfunction +- hemodynamic instability
Chronic: asymptomatic +/- decrease platelet
May be complicated by PE
Diagnosis:
Conventional gray scale US
Duplex US: reversed or absent diastolic flow
MRA with gadolinium or without
Management:
I- Thrombolytic therapy: in chronic TRVT, in acute early postoperative period may be associated with life threatening he
May be used locally combined with percutaneous mechanical thrombectomy in subacute or chronic RVT or when prolonged thrombolysis is contraindicated
II- Surgical thrombectomy require open exploration for evaluation of graft and correction of mechanical factors, effective with early diagnosis.
Prevention:
Proper and meticulous surgical procedure and vascular intervention
Prompt volume state management
Proactive surveillance by daily chemistry, hourly UOP and duplex
Low dose aspirin and LMWH in high risk patients (hypercoagulable state or tx of kidney with more than 1 artery)
Level of evidence: 5
Mahmud Islam
2 years ago
This is last weeks paper.
NOT: VI. Fluid overload in the ICU – evaluation and management
INTRODUCTION
· Postoperative vascular complications occur in 1% to 10% of transplanted patients
· The most common vascular complications are:
1. transplant renal artery stenosis,
2. renal graft arterial or venous thrombosis
3. arterial injury: arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
· Transplant renal vein thrombosis may causes early graft dysfunction after renal transplant, with prevalence of 0.1% to 4.2 % of all transplants
· The prevalence of TRVT is higher in deceased-donor than in living donor transplant
Causes of transplant renal vein thrombosis
1. donor risk factors:
· use of a donor’s right kidney
· Multiple graft vessels
· prolonged ischemia time
· vascular injuries
· Older age of donors
2. Recipient-related risk factors:
· extremes of age
· peritoneal dialysis
· Perioperative hemodynamic status
3. technical issues: kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium
4. mechanical causes:
· a kink in the renal vein
· compression by hematomas or lymphoceles
· anastomotic stenosis
· extension of an underlying deep venous thrombosis
· compression of the renal vein by the renal artery
5. immunosuppression causes:
· cyclosporine, OKT3 antibody
· high doses of pulsed methyl prednisolone
· anti – thymocyte/antilymphocyte globulin
Clinical manifestations of transplant renal vein thrombosis
· rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock
· Chronic vein thrombosis is usually asymptomatic
· Transplant renal vein thrombosis may be complicated by pulmonary embolism, especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins
Diagnosis of transplant renal vein thrombosis
· High clinical suspicion, trigger the use of duplex ultrasonography
· Conventional gray-scale ultrasonography with color and spectral Doppler is used immediately posttransplant to detect complications early
· thrombus in the renal vein is rarely seen on conventional ultrasonographic imaging, due to deep vascular anastomoses
· Duplex ultrasonography characteristically reveals reversed arterial diastolic flow, a spike-like systolic component, and the renal vein non-visualized
· A finding of isolated reversed or absent diastolic arterial flow is sensitive and not pathognomonic and nonspecific to TRVT
· isolated reversed or absent diastolic arterial flow also can be seen in:
1. severe acute rejection
2. severe acute tubular necrosis
3. hematoma
4. vascular kink
· Although angiography remains the criterion standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity
· nuclear medicine scintigraphy or magnetic resonance angiography, offer excellent alternatives without nephrotoxicity and a greater sensitivity than ultrasonography
· MRA can be done without IV contrast
Management of transplant renal vein thrombosis
· Successful emergency surgical thrombectomy has been reported in the early posttransplant period.
· Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period
· Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT
Preventive strategies
· Careful renal retrieval, renal vein repair, and anastomosis and placement of kidney may help to avoide TRVT
· Adequate training in the techniques of vascular anastomosis and graft recovery
· shortening the long renal vein at the time of transplant
· Ipsilateral transplant is preferred.
· Follow up intravascular volume status in recipient
· duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention
Conclusions
· Patients with high risk for TRVT should be followed closely postoperatively
· multidisciplinary team approach may improve outcome in emergency cases
· The prevention of TRVT is more effective than treatment
What is the level of evidence provided by this article?
Narrative review, evidence 5
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Assafi Mohammed
2 years ago
Summary of the article “Transplant Renal Vein Thrombosis”
This article reviewed the transplant renal vein thrombosis(TRVT), which is a devastating vascular complication that may ultimately end with allograft nephrectomy.
· Reported prevalence of 0.1% to 4.2 % of all transplants.
· The prevalence of TRVT is higher in deceased-donor than in living- donor transplant.
· Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases. The most common vascular complications include:
· Transplant renal artery stenosis.
· Renal graft arterial or venous thrombosis.
· Arterial injury; including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas. Causes of transplant renal vein thrombosis
1. Donor-related risk factors:
a) use of a donor’s right kidney; due to:
· the short vein and long artery of the right kidney.
· the right kidney is more difficult to position.
b) Multiple graft vessels.
c) Prolonged ischemia time and vascular injuries.
d) Older age of donors; This is probably because donor hypotension together with ischemia- reperfusion injury may cause the activation of a procoagulant surface from cytokines and the recipient’s immune response with atherosclerotic vessels.
2. Recipient-related risk factors:
a) extremes of age.
b) pretransplant dialysis modality(PD is associated with more graft thrombosis than HD.
c) Perioperative hemodynamic status; hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis.
d) primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
3. Technical issues: ncluding kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
4. Mechanical causes:
· A kink in the renal vein.
· Compression by hematomas or lymphoceles.
· Anastomotic stenosis.
· Extension of an underlying deep venous thrombosis.
· Compression of the renal vein by the renal artery is another risk factor.
5. Immunosuppression-related factors:
· prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti- thymocyte/antilymphocyte globulin.
· Cyclosporine can increase the risk of graft thrombosis due to enhancement of throm- boxane A2 release, thromboplastin generation, platelet aggregation, factor VIII activity, and decreased thrombomodulin activity, hence down-regulation of the protein C anticoagulant pathway.
· Calcineurin inhibitors may also induce hypofibrinolysis by increasing the expression of plasminogen activator inhibitor.
Clinical manifestations of TRVT:
1. The typical clinical presentation:
· rapid onset of oliguria or anuria.
· hematuria with worsening graft function.
· painful swollen graft; which may progress to rupture, hemorrhage, and shock.
2. Chronic vein thrombosis: this is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Diagnosis of TRVT:
1. High clinical suspicion. The clinical diagnosis can be difficult in cases of chronic vein thrombosis, as it is initially asymptomatic.
2. Duplex ultrasonography, it reveals:
a) the reversed or absent diastolic waveform, a sign of extremely high vascular resistance.
· Acute rejection and acute tubular necrosis are the most common differentials for reversed diastolic flow, whereas TRVT remains an uncommon cause of reversed diastolic flow.
b) a spike-like systolic component.
c) non-visualization of the renal vein.
3. Angiography remains the criterion standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
4. Nuclear medicine scintigraphy
5. Magnetic resonance angiography; associated with a risk of NSF in low GFR.
Management of transplant renal vein thrombosis
1. Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy.
· Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
· thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated.
2. The surgical management of vascular complications must include surgical exploration of the allograft.
3. Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT.
Preventive strategies
1. Meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT.
2. Sufficient training in the techniques of vascular anastomosis and graft recovery.
· To shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
· ipsilateral transplant (right to right and left to left) whenever possible.
3. Low-dose aspirin and low-molecular-weight heparin. May be of benefits in high-risk patients:
· Recipients with hypercoagulable profiles.
· Receiver of a kidneys with more than 1 renal artery. What is the level of evidence provided by this article?
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Abdul Rahim Khan
2 years ago
Please summarise this article
The incidence of transplant renal vein thrombosis is from 0.1 to 4.2%. It usually leads to graft loss. It leads to graft nephrectomy in almost all cases.
Aetiology
Use of a donor’s right kidney
Multiple graft vessels
Vascular injuries
Prolonged ischemia
Older age of donors
Recipient Factors
Extremes of age
Peritoneal dialysis is associated with more graft thrombosis than hemodialysis
Hypotension and dehydration
Technical Issues.
A variety of technical issues have also been implicated as risk factors of TRVT
Kinking of the graft vein
Long vein
Wide disparities in vessel size
Injury to the vascular endothelium during surgical manipulation
Mechanical causes- a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis
Prothrombotic immune suppressants
Diagnosis-
Clinical suspicion
Doppler scan
MRI
Treatment
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period
Emergency surgical thrombectomy has been reported in the early posttransplant period
Combined percutaneous mechanical thrombec – tomy and localized catheter-directed thrombolysis
Conclusion
Patients at high risk for TRVT should be identified and followed postoperatively
A meticulous postoperative protocol is critical to graft and patient survival.
A coordinated multidisciplinary team approach is crucial
The prevention of TRVT by careful attention to predisposing factors
What is the level of evidence provided by this article?
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
This is a review article with level evidence of 5.
Summary:
Transplant renal vein thrombosis (TRVT) is an early severe complication of renal transplantation. When chronic can be missed because of being asymptomatic, but when acute, it causes severe pain. In either context, the renal function deteriorates, and the chance of surgical solution is ineffective and usually ends with graft loss and obligatory nephrectomy to avoid shock and other serious adverse effects. Thrombolytic therapy or thrombectomy were reported to be of benefit but may not be curative as it is usually late. Thrombolytic therapy carries the disadvantage of massive haemorrhage.
The most appropriate diagnostic tool is a duplex ultrasound. It has the advantage of being non-invasive, with no harmful contrast and quick.
TRVT can be donor, recipient or surgical-related. the use of the right kidney may be a risk due to short vasculature. multiple vessels anastomosis adds a risk. From the recipient’s point of view, extremes of age, and modality of RRT may potentiate the risk. PD is thought to have more risk in relative to HD because of elevated procoagulant factors. Perioperative volume status, hypovolemia and dehydration carry the risk of AKI and thrombosis. Mechanical factors like kinking of renal vein and compression by hematoma or lymphocele, for example, predispose to thrombosis. injury of the endothelium during surgery is also implicated. contralateral implants (transplanting the right kidney to the left iliac fossa e.g.) may potentiate the risk. Other risks are medication related. OKT, cyclosporin, high-pulse steroid and anti-ATG may play a role.
In conclusion, close monitoring and preventive measures are more important because the treatment itself is mostly unsuccessful and ends with graft loss.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
KAMAL ELGORASHI
2 years ago
Summary of the article;
RVT is rather a critical outcome early occur post operative, and commonly ended by graft loss and nephrectomy. incidence range between 1-4% of all transplanted kidneys and its more common in deceased donation rather than living donation, and this is attributed to fact that living donation may underwent under favorable condition and less ischemic events. Causes;
Donor factors.
Recipient factors.
Operative factors
Immunosuppressants related TRVT.
Donor factor;
Use of donor right kidney, (due to short vein and long artery).
Multiple graft vessels, by some studies.
Prolong IT, and vascular injury.
Old donor age.
Recipient factors;
Extremes of age.
Pre-transplant dialysis modality, (PD ass with higher risk).
Surgical related;
Peri-operative hypotension and dehydration.
Linking of grafted vein.
Long vein.
Disparity of vessel size.
Contralateral procedure, (Rt kidney in the left iliac fossa, and vice versa).
Immunosuppressants related;
Increased risk with prothrombotic drugs, (CyA, OKT3, High dose pulsed methyl prednisolone, and ATG). Clinical manifestation;
Rapid onset of oliguria, anuria.
Hematuria.
Worsening AKI.
Pain full graft swelling, +/- rupture, hemorrhage or shock.
Chronic RVT is usually asymptomatic ass with thrombocytopenia.
PE.
Diagnosis;
Clinical presentation suspicious.
Doppler US.
avoid contrast based imaging, however MRI with no iv contrast is highly valuable.
Dopplex US characteristics;
Reversed arterial diastolic flow.
a spike like systolic component.
Non-invisualized renalvein.
Management;
Thrombolytic therapy, standard for late RVT.
Surgical thrombectomy, for early post-operative RVT.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Rihab Elidrisi
2 years ago
Renal vien thrombosis could be acute or chronic \the acute one usually presented with painful graft and hematuria ,oligoanuric , may progress to rupture, haemorrhage, and shock.
chronic renal thrombosis is usually asymptomatic
Diagnosis is mainly clinical but will need to Doppler of the graft and MRI is the best
managment
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT.
I like your summary and analysis,. You should have typed references.
Ajay
Huda Al-Taee
2 years ago
Summary:
Causes of transplant renal vein thrombosis:
donor risk factors: use of a donor’s right kidney (due to the short vein and long artery of the right kidney), Multiple graft vessels, prolonged ischemia time and vascular injuries, Older age donors.
technical issues: kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
mechanical causes: compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
IS medications like cyclosporine, OKT3 antibody, high doses of pulsed MP, and ATG.
Clinical manifestations of transplant renal vein thrombosis:
The typical clinical presentation: rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, haemorrhage, and shock.
Chronic vein thrombosis is usually asymptomatic.
may be complicated by pulmonary embolism.
Diagnosis:
a highly suspicious clinical presentation.
duplex ultrasonography (reversed diastolic flow).
Conventional gray-scale ultrasonography with color and spectral Doppler.
Magnetic resonance imaging is now considered a reliable tool for the evaluation of renal allografts and the diagnoses of most complications.
Management:
Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy.
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT.
there are no large randomized controlled studies of sufficient power to assess the relative efficacy of different management approaches.
Preventive strategies:
meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in the avoidance of TRVT.
Sufficient training in the techniques of vascular anastomosis and graft recovery is critical.
shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
prefer ipsilateral transplant.
Attention to intravascular volume status.
Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention.
Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Summary: Transplant Renal Vein Thrombosis
Transplant renal vein thrombosis (TRVT) is a devastating complication causing early graft dysfunction, with reported prevalence of 0.1% to 4.2% of all transplants. TRVT leads to graft loss and nephrectomy in almost all cases. It is more common in deceased donor than in living donor. Causes of transplant renal vein thrombosis Donor factors: a- Donor’s right kidney
due to short vein and long artery of the right kidney. The short vein can be easily compressed by kidney swelling due to ischemic damage, acute tubular necrosis, or urinary obstruction. The kidney is more difficult to position especially if multiple renal arteries are present and the long renal artery can be easily kinked. b- Multiple graft vessels c- Prolonged ischemia time which can potentiate thrombogenicity of the endothelium or cause ATN with graft edema that lead decreased perfusion and thrombosis. d- Vascular injuries e- Older age of the donor; due to donor hypotension and ischemia reperfusion injury which cause activation of the procoagulant surface from cytokines response and atherosclerotic vessels.
Recipient-related risk factors
a- Extreme of age especially with the atherosclerotic vessels
b- Variation in the vessels sizes between the donor and recipient, especially with pediatric transplantation.
c- Pretransplant dialysis modality; graft thrombosis is more in peritoneal dialysis than hemodialysis.
d- Hypercoagulable states; as antiphospholipid syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
e- Perioperative hemodynamic status: hypotension cause AKI, hypoperfusin and thrombosis.
f- Primary renal disease like membranous nephropathy. Technical and mechanical issues
a- Kinking of the graft vein,
b- a long vein
c- wide disparities in vessel size
d- injury to the vascular endothelium during surgical manipulation
e- Compression of the vessel by hematoma, or lymphoceles or by renal artery in contralateral transplant procedure, (right kidney into the left iliac fossa and left kidney into the right iliac fossa).
f- Anastomotic stenosis
g- Extension of an underlying DVT
Immunosuppressive drugs
h- Prothrombotic drugs such as cyclosporine, OKT3 antibody, high dose methylprednisolone, and anti –
thymocyte/antilymphocyte globulin. Clinical manifestations of transplant renal veinthrombosis
Usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock. Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus. Urologic complications or acute rejection are important differential diagnosis. Diagnosis of transplant renal vein thrombosis Duplex ultrasonography, Conventional gray-scale ultrasonography with color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and long-term outcomes of noncomplicated renal transplants. Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial wave-form positive during systole and negative during diastole), a spike-like systolic component, and nonvisualization of the renal vein.
There are 3 typical shapes of reversed diastolic waveforms: type 1 or “transient” waveform, in which the reversed diastolic waveform returns to baseline before end diastole; type 2 or “plateau” waveform in which a flat reversed flow remains relatively constant throughout diastole; and type 3 or “inverted M” waveform, in which reversed flow throughout diastole has mid-diastolic deceleration. Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels. Angiography remains the golden standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity. Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications. Management of transplant renal vein thrombosis a- Thrombolytic therapy is usually the treatment of choice for TRVT in the late transplant period. b- surgical thrombectomy in the early post-transplant period. Preventive strategies Technical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, anastomosis and placement of kidneys may hold considerable importance in the avoidance of TRVT.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Heba Wagdy
2 years ago
Post-transplant vascular complications occur in -% of recipients, TRVT is one of the major complications that can lead to graft loss. It is more common in deceased donor transplants due to the associated ischemic injury. Causes of TRVT: Donor related risk factors:
Elderly donors, using donor’s right kidney, multiple graft vessels, prolonged ischemia times and vascular injuries. Recipient related risk factors:
Extremes of age, peritoneal dialysis, hypercoagulable state, hypotension and dehydration preoperatively and primary renal disease as membranous GN. Technical issues:
Kinking of graft vein, compression by hematoma or lymphocele, injury to vascular endothelium, anastomotic stenosis and extension of underlying DVT. Immunosuppressive therapy with prothrombotic effect as cyclosporine, pulse methyl prednisolone and ATG. Clinical manifestations:
Usually asymptomatic, typically present with oliguria, hematuria, deteriorating graft function and painful swollen graft that may progress to rupture and hemorrhage. Diagnosis:
Requires high suspicion Duplex ultrasonography:
Used early post transplant to detect early complications, calculate resistive index and pulsatile index.
Safe, noninvasive with no exposure to radiation or contrast media.
Reveals reversed arterial diastolic flow, spike like systolic component and non visualization of renal vein, with 3 typical shapes of reversed diastolic waveforms, “transient”, “plateau” and “inverted M”.
Isolated reversed or absent diastolic arterial flow is sensitive but not pathognomonic to TRVT.
Diagnosis is affected by patient’s body habitus, operator skills and availability of acoustic window. CT angiography:
Provide definite diagnosis but invasive, use nephrotoxic contrast Nuclear medicine scintigraphy and MR angiography:
More sensitive than U/S, no nephrotoxic agents used.
MR angiography with recent modalities used without contrast and screen for vascular complications.
limited use due to higher cost, long examination time and lack portability. Management: Thrombolytic therapy:
Used late post transplant
May cause life threatening hemorrhage Surgical thrombectomy:
More successful early posttransplant, detect the cause and can correct the technical complications.
Associated with risk of anesthesia and post operative infection. Combined percutaneous mechanical thrombectomy and localized catheter directed thrombolysis were tried safely and effectively.
Success rate of all interventions is variable and long term outcome is not determined. Preventive strategies:
Meticulous surgical techniques, sufficient training in techniques of vascular anastomosis and graft recovery
Shortening of long renal vein to avoid kinking
Ipsilateral transplant whenever possible
Avoiding hypovolemia and hypotension.
Monitoring with duplex ultrasonography during early period post transplant.
Low dose aspirin and LMWH in high risk patients. Level of evidence: 5 (narrative review)
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
abosaeed mohamed
2 years ago
· Introduction:
– The most common vascular complications after kidney transplantation include transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
– Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants. Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases. The prevalence of TRVT is higher in deceased-donor than in living donor transplant. This may be because living-donor transplant procedures are usually done under more favorable conditions and are not usually subjected to ischemic injury
· Causes :
– often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
>> donor risk factors :
– use of a donor’s right kidney is associated with the development of renal graft thrombosis due to the short vein and long artery of the right kidney. The short renal vein can be easily compressed postoperatively by the kidney swelling due to ischemic damage, acute tubular necrosis, or urinary obstruction. The right kidney is more difficult to position, especially if multiple renal arteries are present and the long artery can be easily kinked.
– Multiple graft vessels have been also implicated in renal graft thrombosis in some studies, although refuted in others. In addition, prolonged ischemia time and vascular injuries have been found to be donor risk factors for renal graft thrombosis.
– The prolonged ischemia time could potentiate thrombogenicity of the endothelium, or a resulting acute tubular necrosis with graft edema could lead to decreased perfusion and thrombosis.
– Older age of donors is associated with an in – creased risk of graft thrombosis.This is probably because donor hypotension together with ischemiareperfusion injury may cause the activation of a procoagulant surface from cytokines and the recipient’s immune response with atherosclerotic vessels. >>Recipient-related risk factors:
– extremes of age which may call for more complex surgical procedures, especially with atherosclerotic vessels predisposing to a higher incidence of thrombosis, and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures.
– pretransplant dialysis modality in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
– Perioperative hemodynamic status in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis, and primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis. >>technical issues :
– kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
– a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
– compression of the renal vein by the renal artery is another risk factor, especially in contralateral transplant procedures (right kidney into the left iliac fossa and left kidney into the right iliac fossa).
>>immunosuppression:
– TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti – thymocyte/antilymphocyte globulin.
· Clinical manifestations:
– The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
– Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
– Clinical diagnosis may be easy in cases of acute renal vein thrombosis, although not specific, with diagnosis perhaps confused with the occurrence of a urologic complication or acute rejection, the 2 most frequent complications during the early post – operative period. Transplant renal vein thrombosis may be complicated by pulmonary embolism, especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins
· Diagnosis :
– usually based on a highly suspicious clinical presentation, triggering assessment using duplex ultrasonography.
– The clinical diagnosis can be difficult in cases of chronic vein thrombosis, as it is initially asymptomatic.
– Conventional gray-scale ultrasonography with color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and long-term outcomes of noncomplicated renal transplants . It is noninvasive and is an easily available tool that avoids use of ionizing radiation and iodinated contrast media.
– Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial wave – form positive during systole and negative during diastole), a spike-like systolic component, and nonvisualization of the renal vein . Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels. This high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss. A finding of isolated reversed or absent diastolic arterial flow is sensitive and not pathognomonic and nonspecific to TRVT and may also be seen in an array of causes,such as severe acute rejection, severe acute tubular necrosis, hematoma, and vascular kink. Acute rejection and acute tubular necrosis are the most common causes of reversed diastolic flow, whereas TRVT remains an uncommon cause of reversed diastolic flow.
– MRA without gadolinium contrast is an alternative to angiography .
· Management :
– Successful emergency surgical thrombectomy has been reported in the early posttransplant period. Operative interventions can facilitate better evaluation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.
– Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period >>Preventive strategies :
– meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT. Sufficient training in the techniques of vascular anastomosis and graft recovery is critical, to avoid multiple attempts during the operation and the subsequent iatrogenic vascular trauma.
– A long renal vein is considered a risk factor of , the authors here recommend routinely shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis. also prefer ipsilateral transplant (right to right and left to left) whenever possible and also in cases of short renal vessels (eg, living-donor transplant procedures) to avoid compression of the renal vein by the renal artery.
– Attention to intravascular volume status in patients undergoing renal transplant is recommended. Transesophageal Doppler has been used to monitor the fluid balance during the procedure because it has been more accurate than measurement of central venous pressure.
– Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention may result in successful salvage of a renal allograft
– Some protocols include an hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels.This proactive surveillance approach posttransplant may lead to an early diagnosis, thus allowing salvage of the renal allograft.
– Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients, especially in recipients with hypercoagulable profiles or those who received kidneys with more than 1 renal artery.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Mohammad Alshaikh
2 years ago
Please summarise this article Introduction: Post operative vascular complications in kidney transplantation are major challenges, occur in 1-10% of case and they are: Transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas. Transplant renal vein thrombosis (TRVT) has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a prevalence of 0.1% to 4.2 % of all transplants. Causes of transplant renal vein thrombosis: Donor related: donor’s right kidney is associated with the development of renal graft thrombosis, Multiple graft vessels, prolonged ischemia time, and Older age of donors. Recipient related: older age recipients, variations in vessel sizes between the donor and recipient, pretransplant dialysis modality (peritoneal D > HD), history of thrombophilia, antiphosphlipid antibody, primary memebranous nephropathy, and preoperative hemodynamic status. Perioperative mechanical related: renal vein kinking or compression due to hematoma or lymphocele, extension of underlying DVT, compression of the renal vein by the renal artery especially in contralateral transplant procedures, use of cyclosporine, ATG, and OKT3 antibodies. Cyclopsorin use related is due to enhancement of thromboxane A2 release, and/or induce hypofibrinolysis. Clinical manifestations of transplant renal vein thrombosis: Rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful graft swelling. Thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus, may be complicated by pulmonary embolism. Differential diagnosis are urological complication and acute rejection. Diagnosis of transplant renal vein thrombosis: Ultrasound + duplex ultrasound: suggested when reversed or absent arterial diastolic flow ensue, a spike-like systolic component, and nonvisualization of the renal vein, and very high resistive index. Venography/angiography the gold standard but contrast induced nephropathy of concern. Medical scintigraphy and MRI are used. Management of transplant renal vein thrombosis: As prevention is better than cure preventive measures for decreasing the above mentioned causes of TRVT is a must. Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients. Thrombolytics and thrombectomy is the treatment modalities use early after diagnosis. Unfortunately the end result is graft nephrectomy either due to late diagnosis or failed thrombolytics or thrombectomy. Conclusion: Knowing the risk factors of TRVT, and doing all preventing measures, expertized surgeon, and use of low dose aspirin and low molecular weight heparin early post-transplant can decrease the incidence.
What is the level of evidence provided by this article? Level of evidence V
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. It is level 5 evidence. Ajay
Nahla Allam
2 years ago
Introduction:
Ø Renal transplant is the best option for the treatment of patients with end-stage renal disease
Ø postoperative vascular complications are, occurring in 1% to 10% of transplanted patients
Ø The most common vascular complications :
1- transplant renal artery stenosis,
2- renal graft arterial or venous thrombosis
3- arterial injury, including
I. arteriovenous fistulas,
I. intrarenal pseudoaneurysms,
II. arterial dissection,
III. arterial-calyceal fistulas
Transplant renal vein thrombosis:
The leading causes of early graft dysfunctionafter renal transplant, with a reported prevalence of0.1% to 4.2 % of all transplants.
The prevalence of TRVT is higher in deceased-donor than in living donor transplants.
Causes:
1-donor factors,
2-recipient factors,
3-technical issues during transplant surgery
Donor risk factors:
1-use of a donor’s right kidney.
2-Multiple graft vessels.
3-vascular injuries
4-prolonged ischemia time
5-Older age of donors
Recipient-related risk factors:
1-extremes of age,
2-pretransplant dialysis modality peritoneal dialysis is associated with more graft thrombosis than hemodialysis
3-Peri operative hemodynamic status
4-mechanical causes: Kinking of the grafted vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation
5-administration of prothrombotic drugs such as cyclosporine, OKT3 antibody
Clinical manifestations of transplant renal vein thrombosis:
Ø The typical clinical presentation is usually the rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft
Chronic vein thrombosis is generally asymptomatic.
Diagnosis of transplant renal vein thrombosis:
clinical presentation
duplex ultrasonography
Management of transplant renal vein thrombosis
Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy
Preventive strategies:
1-meticulous surgical techniques
2-Sufficient training in the methods of vascular anastomosis.
3-Attention to intravascular volume status in patients undergoing renal transplant
4-Transesophageal Doppler has been used to monitor the fluid balance during the procedure
5-Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period
6-Low-dose aspirin and low-molecular-weight heparin
Conclusions:
The prevention of TRVT by identify the predisposing factors, including technical
details of surgical procedures, donor and recipient risk factors ,use of heparine and asprine as prophylactic.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. It is level 5 evidence. Ajay
mai shawky
2 years ago
club 6, renal vein thrombosis after KT
Summary:
· Vascular complications occur in 1-10% of renal transplant cases.
· They include renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dis – section, and arterial-calyceal fistulas.
· RVT has detrimental effect on the graft function and causes early graft loss.
· Risk factors for RVT:
o Donor related factors: the donated right kidney with short vein and long artery, especially with multiple renal arteries, prolonged ischemia time that causes the endothelium to be more antigenic, older age of the donors.
o Recipient related factors: older age with atherosclerosis, discrepancy in size of renal vessels between the donor and the recipient especially in pediatric kidney transplantation, procoagulant conditions as antiphospholipid syndrome and inherited coagulopathy, perioperative hypotension that precipitate ATN and graft hypoperfusion and thrombosis, original kidney disease as membranous nephropathy (increased risk of thrombosis), need for dialysis prior to transplantation (especially PD due to accumulation of procoagulant factors than in HD).
o Surgical technique related factors: kinking of the vein or injury to the endothelium.
o Kinking of renal vein or compression of the allograft by hematoma or lymphocele are the common risk factors. Compression of the renal vein by the renal artery is another risk factor, especially in contralateral transplant procedures (right kidney into the left iliac fossa and vice versa).
o Immunosuppression used: high dose steroids, IVIG, OKT3 or ATG. in addition, CNI especially cyclosporine has thrombogenic activity.
· Clinical presentation;
o Acute graft dysfunction (oligo-anuria, hematuria) that is none specific and similar to that of acute rejection and urological complications that are commonly presented early post-transplant period.
o Tender graft that may rupture causing shock.
o consumption thrombocytopenia can be observed few hours after RVT.
o Extension of lower limb DVT usually presented with concomitant pulmonary embolism.
· Diagnosis:
· Abdominal US with color duplex(safe, cheap, available, avoid ionizing radiation and use of nephrotoxic contrast).
o As regard grey scale US: the renal vein is deep in the recipient’s pelvis, thrombus in the renal vein is rarely seen.
o RVT is diagnosed by color duplex by:
· None visualized renal vein.
· Presence of reversed diastolic flow (the wave become negative in diastole below the zero line),
· Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessel which indicates graft dysfunction and is associated with higher incidence of graft loss. however, it is not pathognomonic for RVT.
o Differential diagnosis of reversed diastolic flow early post-transplant (30 days): severe acute rejection, severe ATN, hematoma, and vascular kink. AR and ATN are the most common causes of reversed diastolic flow, whereas TRVT is an uncommon cause.
o Differential diagnosis of reversed diastolic flow late post-transplant ( >30 days): rejection, glomerulosclerosis, low cardiac output).
· Angiography remains the gold standard for the diagnosis of renal vascular pathology, but it is invasive and has significant nephrotoxicity. Hence, nuclear medicine scintigraphy or MRA, is an excellent alternative with better sensitivity than US.
· MRA with gadolinium-based contrast agents is associated with risk of nephrogenic systemic fibrosis in patients with lower GFR. However, imaging modalities have been developed to view the vessels without intravenous contrast. the cost, unavailability, need for anesthesia in children and inaccessibility in critically ill patients are still limitations of MRI.
· Management of RVT:
o Thrombolytic therapy and surgical thrombectomy
o Surgical exploration and graft nephrectomy.
o Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis can be used in none responsive cases.
o Thrombolytic therapy is best in late presentation, has risk of thrombus mobilization and hemorrhage.
o Surgical thrombectomy has risk of anesthesia and infections.
· Prevention is better than cure, due to poor outcome of RVT and inferior outcome of graft salvage procedures, so care about surgical techniques regarding renal retrieval, renal vein repair, and anastomosis are essential to prevent RVT.
o Training on surgical techniques and vascular anastomosis to minimize repeated trial and crashing of vessels, shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis and preference of ipsilateral transplant (right to right and left to left) to avoid renal vein compression by renal artery.
o Optimization of intravascular volume through close monitoring by Transesophageal Doppler (more accurate than measurement of central venous pressure) to prevent graft hypoperfusion.
o Close monitoring of the patient (vital data and urine output), laboratory parametrs of the graft function (creatinine and electrolytes) and duplex (for adequate perfusion of the graft) is essential for early detection and management of any complications.
o Antiplatelet and LMWH can be used for prophylaxis in high risk patients (hypercoaguable state and multiple renal arteries).
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. It is level 5 evidence. Ajay
Abdulrahman Ishag
2 years ago
Introduction;
—————————-
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant . Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.
The prevalence;
—————————–
a reported prevalence of 0.1% to 4.2 % of all transplants. The prevalence of TRVT is higher in deceased-donor than in living- donor transplant.
Causes of transplant renal vein thrombosis;
—————————————————
The pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
Donor risk factors ;
————————
1-use of a donor’s right kidney is associated with the development of renal graft thrombosis, due to the short vein and long artery of the right kidney.
2-The right kidney is more difficult to position, especially if multiple renal arteries are present and the long artery can be easily kinked.
3-Multiple graft vessels have been also implicated in renal graft thrombosis in some studies, although refuted in others.
4-Prolonged ischemia time and vascular injuries have been found to be donor risk factors for renal graft thrombosis.
5- Older age of donors is associated with an in- creased risk of graft thrombosis.
Recipient-related risk factors;
————————————
1-Extremes of age, which may call for more complex surgical procedures, especially with atherosclerotic vessels predisposing to a higher incidence of thrombosis, and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures.
2- Peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
3-Perioperative hemodynamic status, in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis.
4- Primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
Operative factors.
—————————
1-A variety of technical issues have also been implicated as risk factors of TRVT, including; kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
2-The following mechanical causes are considered the most common causes of TRVT: a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
Immunosuppression factors ;
——————————————
TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti-
thymocyte/antilymphocyte globulin.
Clinical manifestations of transplant renal vein thrombosis;
——————————————————————————————————-
The clinical manifestations of acute renal vein thrombosis are nonspecific and are not dissimilar to the features of urine leak, urinary obstruction, or severe acute rejection.
1-The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
2-Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
3-Transplant renal vein thrombosis may be complicated by pulmonary embolism,
especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins.
Diagnosis of transplant renal vein thrombosis;
———————————————————————
The diagnosis of transplant renal vein thrombosis depends on a high index of clinical suspicion and duplex ultrasonographic scans. Although venography remains the criterion standard, this procedure is invasive and nephrotoxic, due to use of ionizing contrast agents and also due to exposure to ionizing radiation.
Management of transplant renal vein thrombosis;
—————————————————————————-
1-Thrombolytic therapy .
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.Thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated.
2-Surgical thrombectomy;
Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state.
3- Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis;
Have been tried safely and effectively in TRVT, notably after the second week after transplant with subacute or chronic TRVT and also in acute TRVT when prolonged thrombolysis has failed or is contraindicated .
The success rate for these interventions is variable among different studies, which are either case or cohort studies. Unfortunately, there are no large randomized controlled studies of sufficient power to assess the relative efficacy of different management approaches.
Preventive strategies;
—————————————-
1-Technical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable impor tance in avoidance of TRVT.
2-Sufficient training in thetechniques of vascular anastomosis and graft recovery is critical, to avoid multiple attempts during the operation and the subsequent iatrogenic vascular trauma.
3- Shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
4- Uses the ipsilateral transplant (right to right and left to left) whenever possible and also in cases of short renal vessels to avoid compression of the renal vein by the renal artery.
5- Attention to intravascular volume status in patients undergoing renal transplant is recommended.
6- Uses strict protocols for postoperative monitoring of the renal allograft to allow prompt, early diagnosis of any complications. Such protocols include an hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels.
7- Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients, especially in recipients with hypercoagulable profiles or those who received kidneys with more than 1 renal artery.
What is the level of evidence provided by this article?
—————————————————————————–
Level V
Hi Dr Ishag, I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. Your headings and sub-headings should be in bold or underline. That will make it easy to read. It is level 5 evidence. Ajay
Hadeel Badawi
2 years ago
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after RT.
The prevalence of TRVT is 0.1% to 4.2 %, and it is higher in DD than in DD transplants.
Causes of transplant renal vein thrombosis Donor risk factors:
The use of the donor’s right kidney due to the short vein and long artery of the right kidney.
Multiple graft vessels.
Prolonged ischemia time.
Vascular injuries.
Older age.
Recipient-related risk factors
Extremes of age>> more complex surgical procedures.
Atherosclerotic vessels.
Variations in vessel sizes between the donor and recipient.
Dialysis modality: PD carries a higher risk.
Hemodynamic status, hypotension and dehydration.
Primary renal disease such as MNP.
Technical issues:
Kinking or compression of the graft vein, a long vein.
Wide disparities in vessel size.
Injury during surgical manipulation.
Immunosuppression:
Prothrombotic drugs such as CsA, OKT3 antibody, IVMP, AtG
Clinical manifestations: Acute RVT: Rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock. Chronic RVT; usually asymptomatic, thrombocytopenia occurs.
Diagnosis:
Duplex ultrasonography
noninvasive and readily available.
No ionizing radiation and iodinated contrast media.
Allows calculation of resistive index and pulsatile index, which may predict graft outcome. Characteristically: Reversed arterial diastolic flow: retrograde blood flow occurred at any time point during the diastole
Sign of vascular resistance.
sensitive and not pathognomonic and nonspecific to TRVT, also seen in rejection, ANT, hematoma, and kinking.
3 typical shapes of reversed diastolic waveforms
type 1 or “transient”: the reversed diastolic waveform returns to baseline before end diastole
type 2 or “plateau”: a flat reversed flow remains relatively constant throughout diastole. Carries a higher rate of graft
loss.
type 3 or “inverted M”; reversed flow throughout diastole has mid-diastolic deceleration.
Angiography is the gold standard for the diagnosis Nuclear medicine scintigraphy Magnetic resonance angiography is more sensitive than US. It has some limitations as it can’t be used in pacemakers, it costs, a long time, and the risk of NSF.
Management of TRVT: Emergency surgical thrombectomy:
In the early transplant period.
Evaluation of the cause of thrombosis
Correction of technical complications
Thrombolytic therapy:
Late transplant period.
Risks; life-threatening hemorrhage, clot migration.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis
Preventive strategies
Meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis.
Shorten the long renal vein at the time of transplant to prevent kinking
Ipsilateral transplant whenever possible
Careful assessment of volume status.
Duplex US monitoring during the early posttransplant period, followed by the timely intervention
Low-dose aspirin and LMWH in a specific population.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. I agree it is level 5 evidence. Ajay
Doaa Elwasly
2 years ago
Introduction The most common vascular complications after transplantation include transplant renal artery stenosis, renal graft arterial or venous throm – bosis, and arterial injury, as AV fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas. Transplant renal vein thrombosis (TRVT) is the main cause of early graft dysfunction after renal transplant. TRVT is more commonly associated with kidneys from deceased donors rather than grafts from living donors due to the exposure to ischemic injury. Causes of transplant renal vein thrombosis · Donor factors Donor’s right kidney is associated with renal graft thrombosis attributed to the short vein which is easily compressed by kidney swelling and long artery of the right kidney which is easily kinked. Multiple graft vessels were implicated in renal graft thrombosis. Prolonged ischemia time and vascular injuries can be superadded factors. Old donor age is accompanied withactivation of a procoagulant surface from cytokines and the recipient’s immune response with atherosclerotic vessels. · Recipient factors Include age extremes with variation in donor and recipient vessel size Pretransplant dialysis modality because peritoneal dialysis is more liable to graft thrombosis rather than hemodialysis due to the hypercoagulable status. Perioperative hypotension and primary renal disease. · Technical issues during transplant As kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium. Compression by hematomas or lymphoceles, Anastomotic stenosis, and extension of DVT. Renal artery can compress the vein in contralateral procedures.
· Surgical factors · Immunosuppression By prothrombotic drugs as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and antithymocyte/antilymphocyte globulin. Clinical picture Rapid onset of oliguria or anuria, hematuria with graft dysfunction, and painful graft that can rupture, causing haemorrhage, and shock. Chronic vein thrombosis is asymptomatic but thrombocytopenia can occur. It can be complicated with pulmonary embolism particularly if associated with DVT. Diagnosis By clinical suspicion ,duplex ultrasonography to evaluate the renal allograft, and calculation of resistive index and pulsatile index to predict short and long term outcomes. Renal vein thrombosis is rarely seen by conventional ultrasonography. Duplex ultrasonography shows reversed or absent arterial diastolic flow which is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels. Reversed diastolic waveforms are either transient , plateau or M shaped. Isolated reversed or absent diastolic arterial flow is sensitive but not pathognomonic to TRVT and can be seen in severe acute rejection, severe ATN , hematoma, and vascular kink. Angiography is invasive and nephrotoxic. Magnetic resonance angiography is a reliable method to screen for vascular abnormalities in renal allografts. IV gadolinium can be eliminated to avoid nephrogenic systemic fibrosis in cases with low GFR. MRI cannot be used for cases with pacemakers and it is expensive with long exam time. Management Thrombolytic therapy , surgical thrombectomy. Thrombolytic therapy can be done in the late transplant period , it is the treatment of choice can be complicated with haemorrhage while Surgical thrombectomy usually done in the early transplant period , it carries risks as that of anesthesia ,infection. Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis can be done after the second week of transplant with subacute or chronic TRVT and in acute TRVT. when prolonged thrombolysis has failed. Prevention Meticulous surgical techniques for renal retrieval, renal vein repair, and anastomosis and placement of kidney are crucial in avoidance of TRVT. As shortening long renal vein at the time of transplant to prevent kinking and subsequent thrombosis and ipsilateral transplant is preferred . Intravascular volume monitoring in renal transplant by transoesophageal doppler. Duplex ultrasonography monitoring during the early posttransplant period and follow up. Strict postoperative monitoring as hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels. Low-dose aspirin and low-molecular-weight heparin can help prevent renal vein thrombosis in high-risk patients. Conclusion Recipients with high risk for TRVT need postoperative follow up to allow early diagnosis and prophylactic measures. MDT is needed to improve graft outcome. Prevention of TRVT is much better than treatment to salvage the graft. – Level of evidence 5
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. I agree it is level 5 evidence. Ajay
Isaac Abiola
2 years ago
SUMMARY
Introduction
Kidney transplantation is the best form of renal replacement therapy, but it also comes with post-transplant vascular complications and top on this list is transplant renal vein thrombosis with prevalence of 0.2% -4.2% and has been reported to be higher in diseased donor than living donor. It’s a complication with very high rate of graft lost even if detected early.
Causes of TRVT
A) Donor riskfactor
use of donor right kidney
multiple graft vessels
older age donor
B) Recipient related risk factor
extreme of age
pre transplant dialysis modality PD > HD
perioperative hemodynamic status
primary renal disease e.g more in MN
C) Mechanical causes
kinking of renal vein
compression by hematoma or lymphocele
anastomotic stenosis
underlying DVT
D) Immunosuppressive causes
cyclosporin
OKT3
High dose of methylprednisolone
Clinical manifestation
rapid oliguria or anuria
hematuria
worsening graft function
painful swollen graft
thrombocytopenia
rupture of graft
pulmonary embolism late complication
Diagnosis of TRVT
High index of suspicion
grey scale ultrasonography with spectral doppler
angiography, drawback is nephrotoxicity
MRI drawback NSF, cost, time consuming
Treatment of TRVT
thrombolytic therapy
surgical thrombectomy
Prevention of TRVT
meticulous surgical technique
adequate training and retraining in vascular anastomosis
avoid use of long renal veins
avoid multiple vessels
close monitoring of urine, Duplex ultrasound and biochemical parameters
use of low dose heparin for those at risk of developing TRVT
Conclusion
Transplant vein thrombosis is among most feared complication because of its lethal outcome graft survival, hence identification of risk factors or causes among donor, recipient, and surgical methods is important in preventing the incidence of TRVT. Moreso, early treatment may be of help in salvaging the graft from complete rejection.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. It is level 5 evidence. Ajay
Riham Marzouk
2 years ago
TRVT
This is post-transplant complications can be happened early with 0.1-4% incidence rate from all transplant, usually diagnosed late as it is clinically similar to urinary obstruction and urine like and even acute rejection, and its diagnosis depends on the clinical suspicion, usually has bad prognosis ends by graft nephrectomy.
Causes of TRVT:
1- Donor factors like old age donor, deceased donor, right kidney as a graft as she has short vein and long artery , also kidney of multiple vessels, prolonged ischemic time, hypotension and ischemia in the donor side can cause ATN and edema inside the graft which predispose to thrombosis.
2- Recipient factors old age recipient due to atherosclerotic vessels , pediatric recipient due to small size vessels, antiphospholipid syndrome, and procoagulant medical condition , primary kidney disease like membranous nephropathy, also modality of dialysis as peritoneal dialysis is associated with circulating pro coagulant factors.
3- Technique related factors vessel injury during anastomosis or nephrectomy, small size vessels or discrepancy in the vessel size, kinked vein.
4- mechanical causes (most common causes of TRVT)
a- kink in the renal vein
b- compression by hematomas or lymphoceles
c- anastomotic stenosis
d- extension of an underlying deep venous thrombosis
5- immunosuppressive medication related factors: CNI, ATG, OKT3, high dose pulse methylprednisolone all are procoagulant or prothrombotic drugs.
Clinically can be manifested by oliguria, anuria, hematuria, elevated renal function, painful graft in acute RVT but the chronic one is asymptomatic.
Diagnosed by:
Conventional gray-scale ultrasonography with color and spectral Doppler which reveals reversed arterial diastolic flow but this picture is nonspecific for RVT and can be seen in cases of ATN, severe acute rejection, hematoma and kinked vessel, so clinical suspicion is very important in diagnosis.
Magnetic resonance imaging MRA is a good tool to evaluate the graft, so imaging without contrast is advised to avoid nephrogenic systemic sclerosis with gadolinium in the patient with low GFR.
How to manage RVT:
1- surgical approach thrombectomy especially in early period post transplant
2- medical approach with thrombolytic therapy especially in the late period
3- Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. I agree it is level 5 evidence, not 4 as per Oxford description of level of evidence. Ajay
Esraa Mohammed
2 years ago
Introduction
*postoperative vascular complications are major challenges, occurring in 1% to 10% of transplanted patients
*The most common vascular complications include transplant renal artery stenosis, renal graft arterial or venous throm -bosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
*Transplant renal vein thrombosis (TRVT) is one of the main causes of early graft dysfunction after renal transplant
Causes of transplant renal vein thrombosis
*multifactorial
includes donor factors,recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
*donor’s right kidney is associated with the devel –
opment of renal graft thrombosis,due to the short vein and long artery of the right kidney
* Multiple graft vessels
*prolonged ischemia time and vascular injuries
*Older age of donors
*Recipient-related risk factors include extremes of age,
pretransplant dialysis modality(in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis) And Perioperative hemodynamic status.
*mechanical causes are considered
the most common causes of TRVT: a kink in the renal
vein, compression by hematomas or lymphoceles,
anastomotic stenosis, and extension of an underlying
deep venous thrombosis.
Clinical manifestations of transplant renal vein
thrombosis
The typical clinical presentation is usually rapid
onset of oliguria or anuria, hematuria with wor –
sening graft function, and a painful swollen graft,
which may progress to rupture, hemorrhage, and
shock
Diagnosis of transplant renal vein thrombosis
*based on a highly suspicious clinical presentation,
triggering assessment using duplex ultrasonography
There are 3 typical shapes of reversed diastolic waveforms: -type 1 or “transient” waveform in which the reversed diastolic waveform returns to baseline before end
diastole
-type 2 or “plateau” waveform in which a flat reversed flow remains relatively constant throughout diastole
-type 3 inverted M” waveform in which reversed flow throughout diastole has mid-diastolic deceleration.
Acute rejection and acute tubular
necrosis are the most common causes of reversed
diastolic flow, whereas TRVT remains an uncommon
cause of reversed diastolic flow.
*Magnetic reso nance angiography is increasingly used to screen for vascular abnormalities in renal allografts
Limitations of magnetic resonance imaging in –
clude the inability to image patients with pace makers,
greater cost, lack of portability, and prolonged
examination time, which is not suited to these
critically ill patients.
Management of transplant renal vein thrombosis
*Two strategies are available thrombolytic therapy and surgical thrombectomy.
*Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
Preventive strategies
*Sufficient training in the techniques of vascular anastomosis and graft recovery is critical, to avoid multiple attempts during the operation and the subsequent iatrogenic vascular
*shorten the long renal vein at the time of transplant to
prevent kinking and subsequent thrombosis.
*ipsilateral transplant
*avoid compression of the renal vein by the renal artery
* clinical assessmentand duplex ultrasonography monitoring during the early posttransplant period
*Low-dose aspirin and low-molecular-weight heparin may also have benefits.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. It is level 5 evidence. Ajay
Ø Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants.
Ø The prevalence of TRVT is higher in deceased-donor than in living donor transplant. This may be because living-donor transplant procedures are usually done under more favourable conditions and are not usually subjected to ischemic injury.
Ø The Pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
Ø Causes of transplant renal vein thrombosis:
donor risk factors:
1. Older age of donors
2. Use of a donor’s right kidney is associated with the development of renal graft thrombosis due to the short vein and long artery of the right kidney.
3. Multiple graft vessels
4. Prolonged ischemia time
Recipient-related risk factors:
1. extremes of age
2. variations in vessel sizes between the donor and recipient
3. pretransplant dialysis modality
4. hypercoagulable states
Technical issues:
1. kinking of the graft vein, a long vein, wide disparities in vessel size
2. and injury to the vascular endothelium during surgical manipulation
Immunosuppression: administration of prothrombotic drugs such as cyclosporine, OKT3 antibody
Ø Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial wave – form positive during systole and negative during diastole), a spike-like systolic component, and non-visualization of the renal vein
Ø Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications. Magnetic resonance angiography is increasingly used to screen for vascular abnormalities in renal allografts
Ø Management of transplant renal vein thrombosis: Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical management of vascular complications must include surgical exploration of the allograft.
Ø Preventive strategies Because graft thrombosis is difficult to treat and graft loss is the usual outcome, development of preventive strategies is of paramount importance. First, technical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT.
Level 5
Causes of transplant renal vein thrombosis
often multifactorial and includes
• donor factors,
• recipient factors,
• technical issues during transplant surged (operative factors),
• and immunosuppression.
• donor risk factors,
1. short vein
2. long artery of the right kidney.
3. multiple renal arteries
4. prolonged ischemia timely
5. and vascular injuries
• Recipient-related risk factors
1. include extremes of age,
2. atherosclerotic vessels
3. variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures
4. peritoneal dialysis
5. antiphospholipid antibody syndrome,
6. antithrombin deficiency,
7. mutation of factor V Leiden,
8. the prothrombin gene.
9. Perioperative hemodynamic status, hypotension and dehydration
10. disease such as membranous nephropathy
A variety of technical issues
the most common causa of TRVT:
1. a kink in the renal vein,
2. compression by hematomas or lymphoceles,
3. anastomotic stenosis,
4. and extension of an underlying deep venous thrombosis.
5. compression of the renal vein by the renal artery, especially in contralateral transplant procedures (right kidney into the left iliac fossa and left kidney into the right iliac fossa).
6. Regarding immunosuppression, cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti- thymocyte/ antilymphocyte globulin.
Clinical manifestations
• The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
• Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur
• Transplant renal vein thrombosis may be complicated by pulmonary embolism,
Differential diagnosis
urologic complication or acute rejection, the most frequent complications during the early post-operative period.
Diagnosis of transplant renal vein thrombosis
a highly suspicious clinical presentation, triggering assessment using duplex ultrasonography
1. It characteristically reveals reversed arterial diastolic flow (ie, the arterial wave- form positive during systole and negative during diastole),
2. a spike-like systolic component,
3. and nonvisualization of the renal vein
Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels.
This high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss
The reversed diastolic wave form was described (in the main or segmental renal arteries), when retrograde blood flow occurred at any time point during the diastole, regardless of whether antegrade flow has happened.
There are 3 typical shapes of reversed diastolic wave form:
type I or “transient” wave form,
the revered diastolic wave form returns to baseline before end diastole;
type 2 or “plateau” waveform,
in which a flat reversed blots remains relatively constant throughout diastole;
and type 3 or “inverted M waveform , in which reversed flow throughout diastole has mid-diastolic deceleration.
A finding of isolated reversed or absent diastolic arterial flogs is sensitive and not pathognomonic and nonspecific to TRVT and may also be seen in
1. severe acute ejection,
2. severe acute tubular necrosis.
3. hematoma.
4. vascular kink
Previous studies have described a plateau-like or inverted M wave form associated with TRVT.
Whereas reversal of flow that is limited to the early diastole has been seen with seven rejection or acute tubular necrosis of the graft.
On the other hand, Lockhart and associates, showed that all waveform types could be present in TRVT patients, and reversed diastolic wave form types were not specific for any cause.
The diagnostic capability of duplex is influenced by
1. the patient’s body habitus,
2. the availability of suitable acoustic windows,
3. the operator’s skill
angiography
remains the standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
nuclear medicine scintigraphy or magnetic resonance angiography,
offer excellent alternatives to the criterion standard with no nephrotoxicity and a greater sensitivity than ultrasonography.
MRI
is considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
MRA
is increasingly used to screen for vascular abnormalities in renal allografts
Due to fear of nephrogenic systemic fibrosis after gadolinium-based contrast agents in patients with decreased GFR, imaging modalities have been developed to view the vessels without intravenous contrast.
Limitations of MRI include
the inability to image patients with pacemakers, greater cost, lack of portability, and prolonged examination time.
Management of transplant renal vein thrombosis
1. Two strategies are available for: thrombolytic therapy
2. surgical thrombectomy.
Successful emergency surgical thrombectomy has been reported in the early posttransplant period.
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT, notably after the second week after transplant )case or cohort studies.), there are no large randomized controlled studies
Preventive strategies
First, technical issues seem to play a major role; therefore,
meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT.
Sufficient training in techniques of vascular anastomosis and graft recovery is critical
A long renal vein is considered a risk factor of thrombosis in the experience of the authors; they routinely shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
They prefer ipsilateral transplant whatever possible and also in cases of short renal vessels
Attention to intravascular volume status
Transesophageal Doppler has been used to monitor the fluid balance during the procedure
duplex monitoring during the early posttransplant period followed by timely intervention
Some transplant centers have used strict protocols for postoperative monitoring:
1. hourly measurement of urine output,
2. daily duplex ultrasonography scanning
3. and daily measurements of serum creatinine and electrolyte levels.
Low-dose aspirin and low-molecular-weight heparin may also have benefits
Level 5
Transplant Renal Vein Thrombosis
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant with a reported prevalence of 0.1% to 4.2%. Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases. The prevalence of TRVT is higher in deceased-donor than in living donor. There are many predisposing factors related to donor, recipient, surgery, and immunosuppression, with mechanical factors being considered the most common causes of transplant renal vein thrombosis. The diagnosis of transplant renal vein thrombosis depends on a high index of clinical suspicion and duplex ultrasonographic scans. Although venography remains the criterion standard, this procedure is invasive and nephrotoxic, due to use of ionizing contrast agents and also due to exposure to ionizing radiation.
Causes of transplant renal vein thrombosis:
The pathogenesis of TRVT is multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
1-Donor factors as donor’s right kidney is associated with the development of renal graft thrombosis due to the short vein and long artery of the right kidney. The short renal vein can be easily compressed postoperatively by the kidney swelling due to ischemic damage, acute tubular necrosis, or urinary obstruction. The right kidney is more difficult to position, especially if multiple renal arteries are present and the long artery can be easily kinked. vascular injuries, The prolonged ischemia time could potentiate thrombogenicity of the endothelium.
2-Recipient factors include extremes of age which may call for more complex sur gical procedures, Other recipient-related risk factors include pretransplant dialysis modality in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene. Perioperative hemodynamic status in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis, and primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
3-Technical issues have also been implicated as risk factors of TRVT, including kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
4-Immunosuppression factors TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti – thymocyte/antilymphocyte globulin.
Clinical manifestations of transplant renal vein thrombosis
The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock. Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours because of platelet sequestration in the thrombus.
Management of transplant renal vein thrombosis Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical management of vascular complications must include surgical exploration of the allograft.
Please summarize this article
The main cause of early renal graft dysfunction is transplant renal vein thrombosis which is commonly seen with deceased donor kidneys because of more exposure to ischemic injury.
TRVT causes:
1- Donor’s right short vein and long artery leads to easily compressed vein with bulky kidney and kinked artery.
2- Donor’s kidney with multiples vessels.
3- Donor with prolonged ischemia and vascular injury.
4- Donor old age.
5- Recipients with extremes of age.
6- Recipients on peritoneal dialysis more than those on hemodialysis.
7- Recipients with peri-operative hypotension.
8- Recipients primary renal disease.
9- Technical issues: kinked graft vein, long vein, disparities in vessel size, vascular endothelial injury, compression by hematoma or lymphocele or renal artery, extension of lower limb DVT.
10- Surgical issues.
11- Immunosuppression: Cyclosporine, OKT3 antibody, ATG.
Clinical diagnosis:
Acute TRVT: oligo-anuric graft failure +/- hematuria, painful graft that might rupture leading to hemorrhagic shock because of intra-abdominal bleeding.
Chronic TRVT: asymptomatic +/- thrombocytopenia.
Imaging:
Duplex USS: reversed or absent arterial diastolic flow.
CT-angiography: invasive and nephrotoxic.
MRA: is reliable method unless contra-indicated because of pacemaker.
Treatment: either thrombolytic therapy or surgical thrombectomy.
What is the level of evidence provided by this article?
Level V
Allograft vein thrombosis is serious problem in the context of kidney transplantation. It occurs early post operatively. Several factors are interplaying, related to donor or recipient, medication and operative procedure. Its incidence: 1-4.2%.
It can lead allograft loss and nephrectomy in almost all cases.
Donors Risk factors:
– Harvesting right kidney: in case of long artery and short vein.
The short vein is vulnerable for consequent compression by swollen allograft secondary to ATN, ischemic and rejection supervene.
Right kidney is difficult to implant than the left one due to possible multiple renal arteries, and long artery could be kinked.
Prolonged cold ischemia time and vascular injury are found to potentiate risk of venous thrombosis. Old aged donors , due to hypotension and resulting reperfusion injury facilitate procoagulant status in atherosclerotic.
Recipients Risk factors :
Extreme of age is a prominent risk factor due to size difference &atherosclerotic changes.
Of note, peritoneal dialysis is more prone for ARVT compare with hemodialysis patients.
Peri-operative hypotension and dehydration might lead to AKI ATN , hypo-perfusion and thrombosis .Membranous nephropathy is associated higher incidence.
Q1- Please summarise this article?
Transplant Renal Vein Thrombosis
Abstract
It is occurs early with prevalence of 0.1% to 4.2%. Associate with bad prognosis with graft loss in almost all cases. predisposing factors related to donor, recipient, surgery, immunosuppression, and mechanical factors is the most common causes.
The clinical manifestations is nonspecific and and should be put in differential diagnosis of urine leak, urinary obstruction, or severe acute rejection.
The diagnosis needs a high index of clinical suspicion and duplex ultrasonography scans. Venography is invasive and nephrotoxic. Treatment: thrombolytic therapy and surgical thrombectomy. The prognosis bad usually end by allograft nephrectomy because delay in diagnosis.
Introduction
postoperative vascular complications occur in 1% to 10% of transplanted operations .
The most common vascular complications include
1) transplant renal artery stenosis,
2) renal graft arterial or venous thrombosis,
3) arterial injury, ( arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas )
presentation is dramatic with early graft dysfunction after renal transplant.
Prevalence of 0.1% to 4.2 % of all transplants. The prevalence is higher in deceased-donor than in living
Donor transplant. Usually end by graft loss and nephrectomy in almost all cases.
Causes of transplant renal vein thrombosis:
When considering donor risk factors:
1) Use of a donor’s right kidney.
2) Multiple graft vessels .
3) Prolonged ischemia time.
4) Vascular injuries.
5) Older age of donors
Recipient-related risk factors include:
1) Extremes of age.
2) Variations in vessel sizes between the donor and recipient.
3) Pre transplant dialysis modality.
4) Peritoneal dialysis.
5) Hypercoagulable states.
6) Perioperative hemodynamic status (hypotension) and dehydration.
7) primary renal disease as membranous nephropathy.
A variety of technical issues:
1) A kink in the renal vein.
2) Compression by hematomas or lymphoceles.
3) Anastomotic stenosis.
4) Extension of an underlying deep venous thrombosis.
Regarding immunosuppression:
1) Prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methylprednisolone, and anti thymocyte / ant lymphocyte globulin.
2) Cyclosporine can increase the risk of graft thrombosis.
Clinical manifestations of transplant renal vein thrombosis:
Typical present as rapid onset of oliguria or a anuria , hematuria with graft dysfunction, and a painful swollen graft which may progress to rupture, hemorrhage and shock. Chronic vein thrombosis is usually asymptomatic. Thrombocytopenia may occur. This complication beside urologic complication and acute rejection are three important causes of early graft dysfunction. May be complicated by pulmonary embolism.
Diagnosis of transplant renal vein thrombosis:
The diagnosis depend on
1) a highly suspicious clinical presentation.
2) triggering assessment using duplex ultrasonography.
Ultrasonography is influenced by
1) The patient’s body habitus.
2) The availability of suitable acoustic windows.
3) The operator’s skill.
Angiography remains the criterion standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
Nuclear medicine scintigraphy or magnetic resonance angiography, are alternatives to the criterion standard with no nephrotoxicity and a greater sensitivity than ultrasonography.
MRI is now considered reliable tool for evaluation of renal allografts and the diagnoses of most complications. Because of nephrogenic systemic fibrosis ( gadolinium induced) imaging modalities have been developed to view the vessels without intravenous contrast.
Limitations of magnetic resonance imaging include
1) The inability to image patients with pace makers.
2) Greater cost.
3) lack of portability.
4) Prolonged examination time.
Management of transplant renal vein thrombosis:
Two treatment strategies are available:
1) Thrombolytic therapy.
2) Surgical thrombectomy.
Operative interventions gives better evaluation of the cause of thrombosis and can allow for the correction of technical complication.
Thrombolytic therapy is usually the treatment of choice in the late transplant period.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively .
Conclusions:
1) Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures.
2) A meticulous postoperative protocol is critical to graft and patient survival.
3) A coordinated multidisciplinary team approach is crucial in improving successful outcomes regarding such complex and urgent situations.
4) The prevention of TRVT, is always more effective than treatment .
Q2- What is the level of evidence provided by this article?
Level of evidence is 5.
Transplant renal vein thrombosis usually occurs early after surgery with a reported prevalence of 0.1% to 4.2%. It is a devastating event that ultimately leads to graft loss in almost all cases. There are many pre disposing factors related to donor, recipient, surgery, and immunosuppression, with mechanical factors being considered the most common causes of transplant renal vein thrombosis.
Transplant renal vein thrombosis (TRVT) of an
allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants. Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.
Causes of transplant renal vein thrombosis The pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression. When considering donor risk factors, use of a
donor’s right kidney is associated with the devel opment of renal graft thrombosis
Recipient-related risk factors include extremes of
age,which may call for more complex sur gical procedures, especially with atherosclerotic vessels predisposing to a higher incidence of thrombosis, and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures. Other recipient-related risk factors include pretransplant dialysis modality,in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene. Perioperative hemodynamic status, in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis, and primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
Clinical diagnosis may be easy in cases of acute
renal vein thrombosis, although not specific, with diagnosis perhaps confused with the occurrence of a urologic complication or acute rejection, the 2 most frequent complications during the early post operative period. Transplant renal vein thrombosis may be complicated by pulmonary embolism, especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins
Diagnosis of transplant renal vein thrombosis The diagnosis of TRVT is usually based on a highly suspicious clinical presentation, triggering assess ment using duplex ultrasonography. The clinical diagnosis can be difficult in cases of chronic vein thrombosis, as it is initially asymptomatic. Conventional gray-scale ultrasonography with
color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and long-term outcomes of noncomplicated renal transplants
Duplex ultrasonography characteristically reveals
reversed arterial diastolic flow (ie, the arterial wave form positive during systole and negative during diastole), a spike-like systolic component, and nonvis ualization of the renal vein. Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels.This high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss
The reversed diastolic waveform was described
(in the main or segmental renal arteries), when retrograde blood flow occurred at any time point during the diastole, regardless of whether antegrade flow has happened.
Magnetic resonance imaging is now considered a
reliable tool for evaluation of renal allografts and the diagnoses of most complications. Magnetic reso nance angiography is increasingly used to screen for vascular abnormalities in renal allografts . Due to fear of nephrogenic systemic fibrosis after gadolinium-based contrast agents in patients with decreased glomerular filtration rate, imaging modalities have been developed to view the vessels without intravenous contrast.
Management of transplant renal vein thrombosis Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical manage ment of vascular complications must include surgical exploration of the allograft. Successful emergency surgical thrombectomy has
been reported in the early posttransplant period. Operative interventions can facilitate better evalu ation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis
Combined percutaneous mechanical thrombec tomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT, notably after the second week after transplant with subacute or chronic TRVT and also in acute TRVT when prolonged thrombolysis has failed or is contraindicated.
Preventive strategies Because graft thrombosis is difficult to treat and graft loss is the usual outcome, development of preventive strategies is of paramount importance. First, tech nical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable impor tance in avoidance of TRVT.
Attention to intravascular volume status in pa tients undergoing renal transplant is recom mended. Transesophageal Doppler has been used to monitor the fluid balance during the procedure because it has been more accurate than measurement of central venous pressure. Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention may result in successful salvage of a renal allograft
Conclusions
Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures. A meticulous postoperative protocol is critical to graft and patient survival. A coordinated multidisciplinary team approach is crucial in improving successful outcomes regarding such complex and urgent situations. The prevention of TRVT by careful attention to predisposing factors, including technical details of surgery procedures, is always more effective than treatment of this dreadful com plication, since it may be too late to salvage a renal allograft once TRVT has been established.
Introduction
Post transplant vascular complication is one of most important challenges , have a prevalence of 1% to 10% and including transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas
Transplant renal vein thrombosis (TRVT) is one of the main causes of early graft dysfunction after renal transplant, with prevalence of 0.1% to 4.2 % .
Causes of transplant renal vein thrombosis :
Clinical manifestations of transplant renal vein thrombosis
Chronic vein thrombosis is usually asymptomatic- thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Diagnosis:
Duplex ultrasonography:
Used early post transplant to detect early complications, calculate resistive index and pulsatile index.
Safe, noninvasive with no exposure to radiation or contrast media.
Reveals reversed arterial diastolic flow, spike like systolic component and non visualization of renal vein, with 3 typical shapes of reversed diastolic waveforms, “transient”, “plateau” and “inverted M”.
Isolated reversed or absent diastolic arterial flow is sensitive but not pathognomonic to TRVT.
Diagnosis is affected by patient’s body habitus, operator skills and availability of acoustic window.
CT angiography:
Provide definite diagnosis but invasive, use nephrotoxic contrast
Nuclear medicine scintigraphy and MR angiography:
More sensitive than U/S, no nephrotoxic agents used.
MR angiography with recent modalities used without contrast and screen for vascular complications.
limited use due to higher cost, long examination time and lack portability.
Treatment of TRVT
There are two treatment options for renal allograft venous thrombosis: thrombolytic therapy and surgical thrombectomy.
Surgical examination of the allograft is required in the therapy of vascular problems.
Thrombolytic therapy is typically the treatment of choice for late-stage TRVT.
Combined percutaneous mechanical thrombectomy and catheter-directed thrombolysis have been tried safely and efficiently in TRVT, particularly after the second week following transplant with subacute or chronic TRVT, as well as in acute TRVT when extended thrombolysis has failed or is contraindicated.
Prevention
Because it may be too late to salvage a kidney transplant after TRVT has formed, prevention of TRVT by paying attention to predisposing variables, such as technical aspects of the surgery, is always more effective than treatment
Introduction:
Postoperative vascular complications are major challenges, occurring in 1% to 10% of
transplanted patients.
The most common vascular complications:
Transplant renal artery stenosis.
Renal graft arterial or venous thrombosis.
Arterial injury:
Including arteriovenous fistulas, intrarenal pseudo aneurysms, arterial dissection, and
arterial-calyceal fistulas.
TRVT:
Prevalence of 0.1% to 4.2 % of all transplants. The prevalence of TRVT is higher in
deceased-donor than in living donor transplant.
Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all
cases.
Causes of transplant renal vein thrombosis:
Donor risk factors:
A donor’s right kidney.
Multiple graft vessels.
Prolonged ischemia.
Vascular injury.
Older age of donors.
Recipient-related risk factors:
Include extremes of age.
Pretransplant dialysis modality, in which peritoneal dialysis is associated with more
graft thrombosis than hemodialysis.
Perioperative hemodynamic status:
Hypotension and dehydration could predispose to acute kidney injury, hypo perfusion,
and thrombosis.
Primary renal disease such:
As membranous nephropathy.
Technical issues:
Including kinking of the graft vein, a long vein, wide disparities in vessel size, and injury
to the vascular endothelium during surgical manipulation.
Mechanical causes:
Are considered the most common causes of TRVT:
A kink in the renal vein, compression by hematomas or lymphoceles, anastomotic
stenosis, and extension of an underlying deep venous thrombosis.
Compression of the renal vein by the renal artery is another risk factor.
Immunosuppression:
Administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses
of pulsed methyl prednisolone, and anti – thymocyte/antilymphocyte globulin AND
Cyclosporine.
Clinical manifestations:
Rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful
swollen graft, which may progress to rupture, hemorrhage, and shock.
Chronic vein thrombosis is usually asymptomatic.
However, thrombocytopenia may occur.
Pulmonary embolism, especially when it is associated with and related to the extension
of deep vein thrombosis.
Diagnosis of transplant renal vein thrombosis:
The diagnosis of TRVT is usually based on a highly CLNICAL suspicious.
Duplex ultrasonography: characteristically reveals reversed arterial diastolic flow (ie,
the arterial wave – form positive during systole and negative during diastole), a spike-like
systolic component, and nonvisualization of the renal vein.
Although angiography remains the criterion standard for the diagnosis of renal vascular
pathology, it is invasive and associated with significant nephrotoxicity.
Other investigations, such as nuclear medicine scintigraphy or magnetic resonance
angiography, offer excellent alternatives to the criterion standard with no nephrotoxicity
and a greater sensitivity than ultrasonography.
Management of transplant renal vein thrombosis:
Two strategies are available for treating venous thrombosis of renal allograft:
thrombolytic therapy and surgical thrombectomy.
Successful emergency surgical thrombectomy has been reported in the early
posttransplant period. Operative interventions can facilitate better evaluation of the
cause of thrombosis and can allow for the correction of technical complications.
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late
transplant period.
Combined percutaneous mechanical thrombectomy and localized catheter-directed
thrombolysis.
level of evidence V.
TRVT
Vascular complications Occurs in 1%to 10% of transplant patients.
Include:
1-Transplant renal artery stenosis
2-Renal arterial or venous thrombosis
3-Arterial injury including AV fistulas , intrarenal pseudo aneurysms, arterial dissection and arterial -calyceal fistulas.
TRVT is one of the main causes of DGF with prevalence of 0.1%_4.2% of all transplants.
Causes :
Multifactorials and include
Donor factors:
Use of Donor right kidney
Multiple graft vessels
Prolonged ischemia time
Vascular injury
Older age donor
Recipient factors:
Extremes of age
Pre transplant dialysis modality, more in PD
Perioperative hemodynamic status
Primary renal disease
Technical issues:
Kinking in graft vein
Long vein
Wide disparities in vessels size
Injury to vascular endothelium
Compression by hematoma or lymphocele
Anastomoses stenosis
Contra lateral transplant procedure
IS factors :
Cyclosporin , OKT3 antibody , high dose of methyl prednisolone and antithymocyte globuline.
Clinical manifestations:
Rapid onset of oliguria or anuria, hematuria with worsening graft function, painful swellen graft which may progress to rupture, hemorrhage and shock.
Chronic vein thrombosis is asymptomatic.
Diagnosis of TRVT:
Is based on highly suspicious clinical presentation.
Conventional gray-scale US with color and Doppler
Finding of isolated reversed or absent diastolic arterial flow is sensitive but not pathognmonic and non specific to TRVT . Acute rejection and ATN also present with reversed diastolic flow.
Angiography remain the criterion standard but it invasive with Nephrotoxicity.
MRI is considered reliable tool for evaluation of renal allograft and most complications.
Management of TRVT:
Thrombolytic therapy
Surgical thromboectomy
Level of evidence:5
Allograft vein thrombosis TRVT:
Allograft vein thrombosis is dreadful encounter in the context of kidney transplantation. Its taking place early post operatively. Multiple factors are interplaying, related to donor, recipient, medication and operative procedure itself.
Incidence: 1-4.2%.
Its resultant in allograft loss and nephrectomy in almost all cases.
Donors Risk factors for ARVT:
1) Harvesting right kidney. Because of long artery and short vein thereof.
The short vein is increasingly vulnerable for consequent compression by swollen allograft secondary to ATN, Ischemic and rejection sequela.
Right kidney is increasingly difficult to implant than the left one due to possible multiple renal arteries, and long artery could be kinked.
prolonged cold ischemia time and vascular injury are reported to potentiate risk of venous thrombosis.
Old aged donors , due to hypotension and reperfusion injury facilitate procoagulant status on atherosclerotic.
Recipients Risk factors for ARVT:
Extreme of age is a prominent risk factor attributed to size difference and atherosclerotic changes.
Interestingly peritoneal dialysis is more prone for ARVT than hemodialysis patients.
Peri-operative hypotension and dehydration might cause AKI ATN , hypo-perfusion and thrombosis .
Membranous nephropathy is linked to higher incidence.
Surgical procedure related risk factors:
long vein is a risk factor for kinking ,
injury to endothelium during manipulation.
Compression by lymphocele and hematoma.
Contralateral transplantation is another risk factor owing to compression by renal artery.
Medications related risk factors for TRVT:
CNi are associated with thrombosis attributed to its thrombogenic tendency , as its increasing liberation of thromboxane A2, thromboplastin, factor VIII platelets aggregability and reduced thrombomodulin.
Presentation:
Acute anuria and oliguric with allograft pain and tenderness with progressive swelling that might progress to rupture and shock .
chronic thrombosis is asymptomatic. Thrombocytopenia might be prominent sign.
pulmonary thromboembolism
Differential Diagnosis:
Acute rejection
Diagnosis:
gray-scale US
Duplex US.
MRI is the best recommended investigation due to limitation of the first 2 modalities.
Preventive measures are best treatment to avoid catastrophic complication of TRVT.
Summary of Transplant Renal Vein ThrombosisIntroduction
Postoperative surgical complication of kidney transplanted patient from 1% to 10%.
Transplant renal vein thrombosis is one of the main causes of early graft dysfunction.
After renal transplant is about 0.1 to 4.2% of all transplants.
Usually RVYT events lead to graft loss and nephrectomy in almost cases.
Causes:
1- Donor factors:
Use donor’s right kidney due to short vein and long artery.
Multiple graft vessels.
Prolong ischemia time.
Vascular injury.
Older age of donor.
2-Recipient -related risk factors:
Extreme age.
Variation in vessels size between the donor and recipient .
Mode of renal replacement therapy more in PD dialysis.
hypercoagulable states.
perioperative haemodynamic status.
primary renal disease like membranous nephropathy.
3-mechnical causes which is common are:
akink in the renal vein .
Compression by hematoma or lymphocele .
anastomotic stenosis.
Extension of an underling deep venous thrombosis.
Compression of renal vein by renal artery especially in contralateral transplant procedure.
Immunosuppression TRVT can be triggered by administration of prothrombotic medication.
Such as cyclosporine CKT3 antibody .high dose of pulse methylprednisolone ,ATG.
Clinical manifestation of RVT:
1- Rapid onset of oliguria or anuria.
2- Haematuria.
3- Worsing graft function.
4- Painful swollen graft.
may progress to rupture haemorrhaged and shock.
Chronic vein thrombosis:
1-asymptomtic
2- thrombocytopenia. Occur in few hours.
Diagnosis of transplant renal vein thrombosis.
Based on highly subspinous clinical presentation.
Duplex u/s
As vascular anastomosis are deep in the recipient pelvis ,thrombus in the renal vein is rarely seen an conventual ultrasound imaging.
Duplex ultrasonography reveals arterial diastolic flow.
Spike -like systolic complement and non visualization of renal vein .
Reversed or absent diastolic flow is assign of extremely high vascular resistance in small interareal artery or large extrarenal vessels .
The high vascular resistance indicate graft dysfunction.
Increased the risk of graft loss.
There are 3 typical shape of reversed diastolic waveform:
1- Type 1 or transient waveform seen in sever rejection or acute tubular necrosis of the graft
2- MRI used to screen vascular abnormalities in renal allograft without i.v contrast but not suitable functional ill patients
Management of transplant renal vein thrombosis:
Two treatment are available for treating venous thrombosis:
1-thrombolytic therapy .
2-surgical thrombectomy.
Successful emergency surgical thrombectomy which is include surgical exploration of the allograft .
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period .
Combined percutaneous mechanical thrombectomy and localized catheter.
Directed thrombolysis is effectively in TRVT.
Prevention strategies:
Sufficient training in the techniques of vascular anastomosis and graft recovery is critical
Avoid long renal vein transplant kidney
Preferable ipsilateral transplant when ever possible.
Use transoesophageal doppler to monitor the fluid balance during the procedure because it has been more accurate.
Conclusion
High risk patients should be followed postoperatively to allow proper diagnosis and prophylactic measures:
Multidisciplinary team approach is crucial in improving successful outcomes such as complex and urgent situation .
Prevent TRVT measurementIncluding technical surgical procedures details.
level evidence 5
.
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants. Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.The prevalence of TRVT is higher in deceased-donor than in living-donor transplant.
CAUSES OF TRANSPLANT RENAL VEIN THROMBOSIS
The pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
Donor risk factors:
– use of a donor’s right kidney
– Multiple graft vessels
– Older age of donos
Recipient-related risk factors
– extremes of age
– pretransplant dialysis modality in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis,
Mechanical causes
– a kink in the renal vein
– compression by hematomas or lymphoceles
– anastomotic stenosis
– extension of an underlying deep venous thrombosis
Prothrombotic drugs
– cyclosporine;
– OKT3 antibody,
– high doses of pulsed methyl prednisolone;
– anti – thymocyte/antilymphocyte globulin
CLINICAL MANIFESTATIONS
The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and Shock. Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
DIAGNOSIS
Conventional gray-scale ultrasonography with color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and long-term outcomes of noncomplicated renal transplants
MANAGEMENT
Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy. The surgical management of vascular complications must include surgical exploration of the allograft.
Successful emergency surgical thrombectomy has been reported in the early posttransplant period. Operative interventions can facilitate better evaluation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.
Thrombolytic therapy is usually the treatment of choice occurring in the late transplant period. Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state, but thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated
Level 05 – narrative review
Allograft vein thrombosis is bit rare complication of transplantation affecting around 2 to 4%. Risk factor could be prolonged ischemia time, old age, right sided donor kidney, perioperative hypotension, kinking of graft vein, raff vascular handling and injury. Usually these patient present with anuria, worsening graft function.
Can be treated with thrombectomy and thrombolysis.
Level V
1. Please summarise this article
Transplant renal vein thrombosis is a serious complication that can end with graft loss. Many risk facors can lead to this and they include: use of a donor’s right kidney, multiple graft vessels, prolonged ischemia, older age of donors, Recipient extremes of age, variations in vessel sizes between the donor and recipient, pretransplant dialysis modality , hypercoagulable states, prothrombotic drugs (such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti thymocyte/antilymphocyte globulin), perioperative hemodynamic status, primary renal disease, kinking of the graft vein, a long vein, wide disparities in vessel size, injury to the vascular endothelium during surgical manipulation, renal veincompression by hematomas or lymphoceles, anastomotic stenosis, extension of an underlying deep venous thrombosis and compression of the renal vein by the renal artery.
Clinical manifestations include rapid onset oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock. On the other hand, chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Diagnosis is usually clinical and through use of duplex ultrasonography. The gold standard method is angiography but it is invasive and is associated with nephrotoxicity. Nuclear medicine scintigraphy or MRA are other alternative diagnostic tools.
Management involves thrombolytic therapy , surgical thrombectomy and combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis .
1. What is the level of evidence provided by this article?
Level V
What is the level of evidence provided by this article?
Level V
Causes of transplant renal vein thrombosis
donor risk factors:
– use of a donor’s right kidney is associated with the development of renal graft thrombosis due to the short vein and long artery of the right kidney
– Multiple graft vessels have been also implicated in renal graft thrombosis
– prolonged ischemic time
– vascular injuries
– Older age of donors is associated with an in – creased risk of graft thrombosis
Recipient-related risk factors
– extremes of age which may call for more complex surgical procedures, especially with atherosclerotic vessels
– pretransplant dialysis modality in which peritoneal dialysis is associated with more
graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable state
– Perioperative hemodynamic status,11,26 in which hypotension and dehydration could predispose to thrombosis
– Regarding immunosuppression, TRVT can also be triggered by administration of prothrombotic
drugs such as cyclosporine, OKT3 antibody
The diagnosis of transplant renal vein thrombosis depends on a high index of clinical suspicion and duplex ultrasonographic scans.
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants.
Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.
When considering donor risk factors, use of a donor’s right kidney is associated with the development of renal graft thrombosis.
prolonged ischemia time and vascular injuries have been found to be donor risk factors for renal graft thrombosis.
Older age of donors is associated with an increased risk of graft thrombosis.
Other recipient-related risk factors include pretransplant dialysis modality, in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis.
The following mechanical causes are considered the most common causes of TRVT: a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
Regarding immunosuppression, TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and antithymocyte/antilymphocyte globulin
Clinical manifestations of transplant renal vein thrombosis
The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial waveform positive during systole and negative during diastole), a spike-like systolic component, and nonvisualization of the renal vein
Successful emergency surgical thrombectomy has been reported in the early posttransplant period. Operative interventions can facilitate better evaluation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.11,55,56
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period. 57-60 Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state, 54 but thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated.55,61 However, this is not the case in every patient; there are reports of successful thrombolytic therapy in the early posttransplant period.54
Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures. A meticulous postoperative protocol is critical to graft and patient survival. A coordinated multidisciplinary team approach is crucial in improving successful outcomes regarding such complex and urgent situations. The prevention of TRVT by careful attention to predisposing factors, including technical details of surgery procedures, is always more effective than treatment of this dreadful complication, since it may be too late to salvage a renal allograft once TRVT has been established.
level V
Transplant renal vein thrombosis usually occurs early after surgery with a reported prevalence of 0.1% to 4.2%.
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant
The prevalence of TRVT is higher in deceased-donor than in livingdonor transplant
Causes of transplant renal vein thrombosis
Donor factors right kidney , Multiple graft vessels , Prolonged ischemia time , Vascular injury
Old age
Recipient factorsn old age , Pretransplant dialysis modality , Perioperative hemodynamic status
Primary renal disease
Mechanical factors Kinking of graft vein, compression , Long vein , Wide disparities in vessel size
Injury to the vessels during surgical manipulation
Immunosuppression medx Cyclosporin , High doses of methylpred , ATG
Clinical manifestation
Rapid onset of oliguria or anuria, hematuria , worsening graft function,
thrombocytopenia
Complications :pulmonary embolism and DVT
Diagnosis:
– duplex Ultrasonography
It can reveal reversed arterial diastolic flow (arterial wave form positive during systole and negative during diastole)
Reversed diastolic flow is a sign of extremely high vascular resistance.
– Angiography :Invasive and carry a risk of nephropathy
-Nuclear medicine scintigraphy
-MRA
Management
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant
period. can cause life-threatening hemorrhage
Surgical thrombectomy has risks associated with anesthesia and postoperative infection
in an immunosuppressed state,
Combined percutaneous mechanical thrombectomy and localized catheter directed thrombolysis: safe and effective
level of evidence 5
Transplant renal vein thrombosis: (TRVT)
This complication occurs in the early post operative phase usually within 4 weeks of surgery… The incidence of this devastating complication is 0.1-4.2% …. It is one of the main complications after surgery leading to acute graft dysfunction and graft nephrectomy in the major of the cases… It also is a clinical masquerader to urine leak, urinoma and lymphocele…
Causes of TRVT: The causes of TRVT include a multifactorial approach namely
clinical signs:
Sudden onset of graft pain and tenderness with oliguria and hematuria is described as the classical signs of TRVT. If not identified it may progress to shock and graft rupture..chronic renal vein thrombosis maybe asymptomatic…Sometimes clinical diagnosis maybe skewed when TRVT is associated with acute rejection or lymphocele.. One should always be vigilant for the development of pulmonary embolism..
Diagnosis:
Ultrasound may show decreased echoes of the kidneys due to edema of the kidney…Duplex ultrasound has been shown to be diagnostic of the condition…It shows reversed arterial diastolic flow (positive during systole and negative during diastole) and spike like systolic component. .There are 3 types of reversed diastolic flow in the graft//Transient reversal/ Plateau type/ M type reversal…Absent of reversed diastolic flow is sensitive but not specific for the TRVT. It can be seen in advanced graft rejection, severe ATN, or severe compression or kink by the any external collection…visualization of the thrombus by USG doppler is challenging as it may be deep
CT angiography can diagnose the condition but it required exposure to contrast with risk of graft injury…..MR angiography is non nephrotoxic and can pick up RVT. Scintigraphy studies also known to identify the condition….
Surgical treatment of RVT involves graft thrombectomy either catheter directed or mechanical means of catheter directed, but these procedures are not associated with success…
Medically patients must be on IV heparin and long term anticoagulation is indicated…serial repeated doppler can tell if the RVT is resolving….
Unfourtunate cases of graft nephrectomy have been done after extensive TRVT.. Preventive techniques by enhancing surgical enterprise and low dose aspirin with LMWH have been implicated to prevent TRVT in high risk cases like multiple vessels
this is a review article is level 5 ..review article or expert opinion
Renal vein thrombosis
It’s a common problem post transplant.
It’s account 1 to 10% transplant patients.
Other common vascular complications post transplant are,
transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
Renal vein thrombosis is the main cause of early graft dysfunction and graft loss and nephrectomy.
There’s many causes of renal vein thrombosis related to donor and recipient and technical issues.
Donor causes:
Right kidney associated with renal vein thrombosis because of short vein and long artery.
Multiple vessels of graft predispose graft to vascular injury and acute tubular necrosis and urine obstruction.
Older donor also lead to renal vein thrombosis.
variations in vessel sizes between the donor and recipient.
Extreme age of recipient and hemodynamic instability like hypotension and dehydration.
Pretransplant dialysis modalities because peritoneal dialysis more prone to renal vein thrombosis more than haemodialysis.
primary renal disease like membranous nephropathy.
Technical issues like kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
Immunosuppressive therapy like cyclosporine induced renal vein thrombosis post transplant.
Clinical manifestations of transplant renal vein
thrombosis.
Anuric or oliguria with hematuria and rapid deterioration of graft function and severe graft pain.
It’s may complicated to pulmonary embolism.
Diagnosis by duplex ultrasonography.
it’s safe and noninvasive shows plateau like or inverted M waveform.
Renal angiography is diagnostic but invasive and nephrotoxic.
Other helpful in diagnosis and less nephrotoxic nuclear medicine scintigraphy or magnetic resonance angiography.
Magnetic resonance imaging but limited in patients with low eGFR because gadolinium toxicity and also limited in patients with pacemaker.
Treatment of renal vein thrombosis:
Anti thrombolytic therapy and surgical thrombectomy but thrmolytic therapy carries risk of bleeding.
Combined percutaneous mechanical thrombec- tomy and localized catheter directed thrombolysis is used now safely.
Prevention of renal vein thrombosis:
Good training for vascular anastomoses of renal vessels during operation to avoid vessel injury and damage or kink.
routinely shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
Good assessment of volume status and good hydration
Dail assess urine output and creatinine level and electrolytes.
Daily doppler ultrasound post transplant in first weeks for timely diagnosis.
Low dose aspirin and low molecular weight heparin especially in patients with hypercoagulablity status.
Transplant renal vein thrombosis
Post operative vascular complications considered major challenge during renal transplant surgery, occurs 1-10% of the kidney transplant.
1. These complications includes renal artery stenosis
2. Renal allograft arterial or venous thrombosis
3. Arterial injury such are
· arterial AV fistulae,
· intrarenal aneurysm,
· arterial dissection,
· arterial -calyceal fistulas.
Causes of transplant RVT
1. Donor factors
· Donors rt kidney (short vein, long artery)
· Multiple graft vessels
· Prolonged ischemia
· Vascular injury
· Old age of donors (hypotension, ischemic reperfusion)
2. Recipient factors
· Extremes of age (elderly -atherosclerotic vessels, pediatric with variation in vessel sizes between the donor and recipient).
· Pretransplant dialysis modality (PD associated with RVT due to high procoagulant factor, hypercoagulable state)
· Perioperative hemodynamic status (hypotension, dehydration).
· Primary renal disease such as membranous GN
3. Technical factors
Kinking of graft vein, compression by hematoma /lymphocele/anastmotic stenosis
Long vein
Wide disparities in vessel size
Injury to the vascular endothelium during surgical manipulation
Compression of the renal vein by the renal artery esp. in the contralateral transplant procedure (rt kidney in lt iliac fossa)
4. Immunosuppressant
Prothrombotic drugs such as
Cyclosporin
OKT3 antibody
High doses of pulse steroid
ATG
Clinical manifestation of transplant RVT
Rapid onset of oliguria or anuria, hematuria , worsening graft function, painful swollen graft prone for rupture or hemorrhage.
In chronic RVT thrombocytopenia as a consequence of platelets sequestration.
The clinical presentation can be confused with urological complications.
Diagnosis:
Depends on highly suspicious clinical presentation
Requires duplex Ultrasonography
(conventional gray scale ultrasonography with color and spectral doppler, with calculation of resistive index and pulsatile index)
It can reveal reversed arterial diastolic flow (arterial wave form positive during systole and negative during diastole)
Reversed diastolic flow is a sign of extremely high vascular resistance.
Angiography :Invasive and carry a risk of nephropathy
Other considered excellent alternative with no nephrotoxicity
Nuclear medicine scintigraphy
MRA
MRI is also reliable tool however there is a fear of nephrogenic systemic fibrosis. Its limitations include greater cost lack of portability and prolong examination time also cant be used in patients with pacemakers.
Management of transplant RVT
· Thrombolytic therapy: treatment of choice for transplant RVT however it can be associated with life threatening hemorrhage/ clot migration.
· Surgical thrombectomy: has risk of anesthesia, post operative infection
· Combined percutaneous mechanical thrombectomy and localized catheter directed thrombolysis: safe and effective
Preventive strategies:
5. Sufficient training
6. Avoid long renal vein
7. To do Ipsilateral transplant
8. Attention to intravascular volume
9. Use of ultrasound foe early monitoring
10. To use postoperative protocols to monitor for
· Hrly urine output
· Daily duplex uss
· Daily serum creatinine and electrolytes
· Low dose aspirin
· Low molecular weight heparin
level of evidence 5
Transplant renal vein thrombosis is a rare complication of kidney transplant affecting 1 to 4.2% of patients.
Risk factors are
Donor driven
Right sided donor kidney having short renal vein.
Prolonged ischemia time.
Old age of donor.
Recipient related risk factors include
Extremes of age.
Peritoneal dialysis
Perioperative hypotension and dehydration.
Technical Risk factors
kinking of graft vein
Long vein
Injury to vascular endothelium during surgical manipulation.
Compression of renal vein by renal artery is another risk factor especially in contra lateral transplant procedures.
Amongst immunosuppression Cyclosporine can increase the risk
CLINICAL MANIFESTATIONS
Oliguria or anuria
Hematuria with worsening graft function
chronic renal vein thrombosis is usually asymptomatic.
DIAGNOSIS OF RVT
Color Doppler ultrasound is easily available and non invasive way of diagnosis.
Reversed diastolic flow is suggestive though it can also be seen in ATN, acute rejection, hematoma and vascular Leak.
CT angio
Renal scan
MRI are other means of diagnosis each having its own pros and cons.
MANAGEMENT
The key point in management is early diagnosis
Thrombolytic therapy is usually treatment of choice
Surgical exploration and thrombectomy is another alternative.
Combined percutaneous mechanical thrombectomy and Localized catheter directed thrombolysis have been tried safely and effectively.
CONCLUSION
High risk patients should be identified.
Meticuolous post transplant protocol should be adopted for early diagnosis and intervention.
A coordinated multidisciplinary approach is needed to manage such patients.
INTRODUCTION
Transplant vein thrombosis is a catastrophic event in terms of long term graft survival. It causes graft loss in almost all cases.
Prevalence of the disease is usually 0.1 to 4.2 %. there are number of post operative vascular complications in transplanted patients. The most common are:
CAUSES OF TRANSPLANT RVT
DONOR FACTORS
RECIPIENT RISK FACTORS
MECHANICAL CAUSES
IMMUNOSUPPRESSION – Cyclosporine
CLINICAL FEATURES
DIAGNOSIS
MANAGEMENT
patients who are at high risk of developing transplant vein thrombosis should be meticulously followed up post operatively sop that prompt diagnosis and necessary measures can be taken timely.
The prevention of TRVT by careful attention to predisposing factors, including technical details of surgery procedures, is always more effective than treatment of this dreadful complication.
# Please summarise this article
* Transplant renal vein thrombosis usually occurs early after surgery with a reported prevalence of 0.1% to 4.2%. It is leads to graft loss in almost all cases.
# Causes of transplant renal vein thrombosis
The pathogenesis are multi-factorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
# The donor risk factors:
1 *Use of a donors right kidney is associated with the development of renal graft thrombosis( due to the short vein and long artery of the right kidney).
2*Multiple graft vessels
3*Prolonged ischemia
4*Older age of donors
# Recipient risk factors:
1*Extremes of age especially with atherosclerotic vessels and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures.
2*Peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
3*Hypotension and dehydration
# Technical factors
1*Kinking of the graft vein
2*Long vein
3*Wide disparities in vessel size
4*Injury to the vascular endothelium during surgical
manipulation.
*The following mechanical causes are considered the most common causes of TRVT:
* Kink in the renal vein,
* Compression by hematomas or lymphoceles,
* Anastomotic stenosis
*Extension of an underlying DVT
*Compression of the renal vein by the renal artery is another risk factor, especially in contra-lateral transplant procedures
# Regarding
immunosuppression factor:
*TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and ATG.
#Clinical manifestations of TRVT
*Rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
*Chronic vein thrombosis is usually asymptomatic, but thrombocytopenia may occur after a few hours
# Clinical diagnosis
*The diagnosis of TRVT is usually based on a highly suspicious clinical presentation,
*Duplex ultrasonography.
*Nuclear medicine scintigraphy or magnetic resonance angiography, offer excellent alternatives to the criterion standard with no nephrotoxicity and a
greater sensitivity than ultrasonography.
*Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
#Management of TRVT
*Two strategies are available:
A* Thrombolytic therapy: is usually the treatment of choice for TRVT occurring in the late transplant period.
B*Surgical thrombectomy: successful emergency surgical thrombectomy has
been reported in the early post-transplant period.
* Operative interventions can facilitate better evaluation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.
C*Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT
# Conclusions
*Patients who are at high risk for TRVT should be identified and followed postoperatively to allow prompt diagnosis and prophylactic measures.
* A meticulous postoperative protocol is critical to graft and patient survival.
*A coordinated MDT approach is crucial
* The prevention of TRVT by careful attention to predisposing factor, including technical details of surgery procedures.
# What is the level of evidence provided by this article?
*Level 5
Introduction:
Transplant renal vein thrombosis (TRVT) is one of the leading causes of early graft malfunction following renal transplant, affecting 0.1% to 4.2% of all transplants. Transplant renal vein thrombosis nearly always causes graft loss and nephrectomy.
Risk Factors:
-Related to the donor:
using Rt kidney, Multiple graft vessels, prolonged ischemia time, vascular injuries, and Older age.
-Related to the recipient:
extremes of age, pretransplant dialysis modality, in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, hypotension, dehydration, and primary renal disease such as membranous nephropathy.
-technical issues:
kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and DVT extension. The renal artery compressing the renal vein is another risk factor., for a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
Regarding immunosuppression:
cyclosporine, OKT3 antibody, high doses of pulsed methylprednisolone, and anti-thymocyte/anti-thymocyte globulin.
Transplant renal vein thrombosis symptoms:
Rapid onset oliguria or anuria, hematuria with worsening graft function, and a painful swelling graft may lead to rupture, bleeding, and shock.
Asymptomatic chronic vein thrombosis. Platelet sequestration in the thrombus may cause thrombocytopenia within a few hours.
Renal vein thrombosis diagnosis:
A worrisome clinical presentation triggers duplex ultrasonography to diagnose TRVT. Duplex ultrasonography shows reversed arterial diastolic flow, a spike-like systolic component, and non visualization of the renal vein.
Renal vein thrombosis management:
Thrombolytic treatment and surgical thrombectomy may treat renal allograft thrombosis. Vascular problems must be treated with allograft exploration.
-Prevention of TRVT by paying attention to predisposing variables, including technical specifics of the surgery, is always more successful than therapy, because it may be too late to salvage a kidney allograft once TRVT has developed.
Level of evidence V, narrative review.
Transplant Renal Vein Thrombosis
Causes
Donor factors:
Recipient-related risk factors
Technical and mechanical issues
Compression of the vessel by hematoma, or lymphoceles or by renal artery in contralateral transplant procedure-right kidney into the left iliac fossa and left kidney into the right iliac fossa.
Anastomotic stenosis
Extension of an underlying DVT
Immunosuppressive drugs
Clinical manifestations of transplant renal vein thrombosis
Chronic vein thrombosis is usually asymptomatic- thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Diagnosis of transplant renal vein thrombosis
Duplex ultrasonography, Conventional gray-scale ultrasonography with colour and spectral Doppler – early detection of complications and evaluation of the renal allograft- allows calculation of resistive index and pulsatile index
Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial wave-form positive during systole and negative during diastole), a spike-like systolic component, and nonvisualization of the renal vein.
There are 3 typical shapes of reversed diastolic waveforms:
Angiography remains the golden standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
MRI is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
Management of transplant renal vein thrombosis
Thrombolytic therapy is usually the treatment of choice for late transplant period.
surgical thrombectomy in the early post-transplant period.
Narrative review level 5
Transplant Renal Vein Thrombosis
______________
Summary
♧ Introduction
▪︎One of the most common vascular complications after renal transplantation is transplant renal vein thrombosis (TRVT) and it is
one of the main causes of early graft dysfunction, with a reported prevalence of 0.1% to 4.2 % of all transplants which is higher deceased-donor than in living donor. It’s events lead to graft loss and nephrectomy in almost all cases.
◇ Causes of transplant renal vein thrombosis ▪︎Includes: donor factors,
recipient factors, technical issues during transplant
surgery (operative factors), and immunosuppression.
Donor- related risk factors:
1. Use of a donor’s right kidney (due to the short vein and long artery of the right kidney).
2. Multiple graft vessels
3. Prolonged ischemia time
4. Vascular injuries
5. Older age
Recipient-related risk factors:
1. Extremes of age
2. Peritoneal dialysis
3. Perioperative hemodynamic status which cause acute kidney injury, hypoperfusion, and thrombosis
4. Primary renal disease such as membranous
Technical issues:
1. Kinking of the graft vein or a long vein
2. Wide disparities in vessel size.
3. Injury to the vascular endothelium
Mechanical causes:
1. Kink in the renal vein
2. Compression by hematomas or lymphoceles.
3. Anastomotic stenosis.
4. Extension of an underlying DVT.
5. Compression of the renal vein by the renal artery, especially in contralateral transplant procedures (right kidney into the left iliac fossa and left kidney into the right iliac fossa).
Immunosuppression:
1. Administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and ATG.
Clinical manifestations of transplant renal vein thrombosis
▪︎The typical clinical presentation is usually rapidonset of oliguria or anuria, hematuria with wor ▪︎Sening graft function, and a painful swollen graft,
which may progress to rupture, hemorrhage, and
shock.
▪︎Chronic vein thrombosis is usually asymp –
tomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet
sequestration in the thrombus.
◇ Differential diagnosis of acute TRVT,
1. Urologic complication.
2. Acute rejection
Complication of TRVT: pulmonary embolism,
Diagnosis of transplant renal vein thrombosis
1. Clinical diagnosis (can be difficult in cases of chronic vein thrombosis).
2. Duplex ultrasonography.
3. Conventional gray-scale ultrasonography with color and spectral Doppler
4. Angiography but it is invasive and associated with significant nephrotoxicity.
5. Nuclear medicine scintigraphy or MRA, offer excellent alternatives to the criterion standard with no nephrotoxicity and a
greater sensitivity than ultrasonography.
▪︎Limitations of magnetic resonance
i. Inability to image patients with pace makers,
ii. Greater cost
iii. Lack of portability.
iv. Prolonged examination time.
Management of transplant renal vein thrombosis
Two strategies
1.Thrombolytic therapy
2. Surgical thrombectomy.
3. Combined percutaneous mechanical thrombec –
tomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT, notably after the second week after transplant with subacute or chronic TRVT and also in acute TRVT when prolonged thrombolysis has failed or is contraindicated.
Preventive strategies
1. Sufficient training in the techniques of vascular anastomosis and graft recovery is critical.
2. Avoid multiple attempts during the operation.
3. Shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
4. Ipsilateral transplant whenever possible and also in cases of short renal vessels.
5.Attention to intravascular volume status
6. Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention.
7. Strict protocols for postoperative monitoring (an hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels.
8. Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients.
♧ Level of evidence: V
● The most common vascular complications
** transplant renal artery stenosis
** renal graft arterial or venous thrombosis
** arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas
● Transplant renal vein thrombosis
** prevalence of 0.1% to 4.2 %
** lead to graft loss and nephrectomy in almost all cases
** The prevalence is higher in deceased-donor than in living-donor transplant.
This may be because living-donor
● Causes of transplant renal vein thrombosis:
** technical issues during transplant
** surgery (operative factors)
** donor’s right kidney
** Multiple graft vessels
** prolonged ischemia time
** Older age of donors
** Recipient extremes of age
** variations in vessel sizes between the donor and recipient
** pretransplant dialysis modality peritoneal dialysis is associated with more
graft thrombosis than hemodialysis
** elevated plasma procoagulant factors, hypercoagulable states,
** Perioperative hemodynamic status,
hypotension and dehydration could
** primary renal disease such as membranous nephropathy
** technical issues including kinking of the graft vein, a long vein wide disparities in
vessel size, and injury to the vascular endothelium
** contralateral transplant procedures
** drugs such as cyclosporine, OKT3 antibody, pulsed methyl prednisolone, and anti -thymocyte/antilymphocyte globulin
● Clinical manifestations :
** rapid onset of oliguria or anuria,
** hematuria
** worsening graft function
** a painful swollen graft,
** Chronic vein thrombosis is usually asymptomatic.
** thrombocytopenia after a few hours
Complications as urologic complication or acute rejection, pulmonary embolism,
● Diagnosis of TRVT is based on
** a highly suspicious clinical presentation,
** duplex ultrasonography with calculation of resistive index and pulsatile index,
** high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss
** Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
● Limitations of magnetic resonance imaging include
** inability to image patients with pace makers
** greater cost
** lack of portability
** prolonged examination time
● Management of transplant renal vein thrombosis
Two strategies are available :
** thrombolytic therapy
** surgical thrombectomy
● Thrombolytic therapy is usually the treatment of choice for TRVT in late period but thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated
● Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state
● Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT,
● Preventive strategies
** Sufficient training in the techniques of
vascular anastomosis
** A long renal vein is considered a risk factor of thrombosis
** ipsilateral transplant whenever possible
** Attention to intravascular volume status
** Transesophageal Doppler to monitor the fluid balance during the procedure
** clinical assessment and duplex ultrasonography monitoring during the
early posttransplant period
** Low-dose aspirin and low-molecular-weight heparin in high-risk patients
● Level 5
SUMMARY:
INTRODUCTION:
One of the major challenges of kidney transplantation is post-operative vascular complications. The vascular complication can occur in about 1-10% of cases. They are:
1) Renal artery stenosis
2) Renal graft arterial or venous thrombosis
3) Intrarenal pseudoaneurysms
4) Arterial dissection and
5) Arterial calyceal fistulas
The article focuses on transplant renal vein thrombosis (TRVT) and which is one of the main causes of graft dysfunction after kidney transplantation. It can be occurring about 0.1-4.2% of all transplants.
The causes of TRVT are:
1) Donor related. Factors like prolonged ischemia time, older age, and multiple graft vessels can cause venous thrombosis
2) Recipient related. Factors like old age, antiphospholipid antibody, primary membranous nephropathy, and preoperative hemodynamic status.
3) Perioperative mechanical factors like hematoma that may cause compression, renal vein kinking, use of medications like ATG, cyclosporine, etc.
The diagnosis of TRVT:
1) The use of ultrasound and or duplex ultrasound
2) Venography/angiography
3) Medical scintigraphy
4) MRI
The management of TRVT:
Prevention of risk factors must be avoided or treated.
Starting of aspirin and or low molecular weight heparin
Thrombolytics and thrombectomy
Nephrectomy is the last resort if all fails
So in conclusion, preventing the risk factor is important. The cause needs to be treated. Once it has been diagnosed, treatment must be initiated like aspirin, and low molecular heparin to ensure to eliminate the thrombosis and to try to ensure the graft survives.
The level of the article is level 5
Renal vein thrombosis complicates 0.1-4.2% of renal tx operations.
It is a devastating complication and usually ends with graft nephrectomy.
Causes often multifactorial
– Donor related:
I. rt kidney donation: short vein could be compressed by swollen kidney
II. Prolonged ischemia increases the thermogenic ability of the endothelium
III. Multiple vessels is controversial
IV. Vascular injuries.
V. Older age.
– Recipient factors:
a. Older age and pediatric
b. Hypercoagulable state
c. PD more than HD
– Operation-related:
a. Renal vein kinking especially in contralateral tx
b. Compression by hematoma
– Immunosuppression:
CNI, high dose methylprednisolone and ATG
Clinical manifestation:
Acute: Oliguria or anuria, painful tender graft, graft dysfunction +- hemodynamic instability
Chronic: asymptomatic +/- decrease platelet
May be complicated by PE
Diagnosis:
Conventional gray scale US
Duplex US: reversed or absent diastolic flow
MRA with gadolinium or without
Management:
I- Thrombolytic therapy: in chronic TRVT, in acute early postoperative period may be associated with life threatening he
May be used locally combined with percutaneous mechanical thrombectomy in subacute or chronic RVT or when prolonged thrombolysis is contraindicated
II- Surgical thrombectomy require open exploration for evaluation of graft and correction of mechanical factors, effective with early diagnosis.
Prevention:
Proper and meticulous surgical procedure and vascular intervention
Prompt volume state management
Proactive surveillance by daily chemistry, hourly UOP and duplex
Low dose aspirin and LMWH in high risk patients (hypercoagulable state or tx of kidney with more than 1 artery)
Level of evidence: 5
This is last weeks paper.
NOT: VI. Fluid overload in the ICU – evaluation and management
Claure-Del Granado and Mehta BMC Nephrology (2016) 17:109 DOI 10.1186/s12882-016-0323-6 link:
https://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-016-0323-6
I will add summary later:
INTRODUCTION
· Postoperative vascular complications occur in 1% to 10% of transplanted patients
· The most common vascular complications are:
1. transplant renal artery stenosis,
2. renal graft arterial or venous thrombosis
3. arterial injury: arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
· Transplant renal vein thrombosis may causes early graft dysfunction after renal transplant, with prevalence of 0.1% to 4.2 % of all transplants
· The prevalence of TRVT is higher in deceased-donor than in living donor transplant
Causes of transplant renal vein thrombosis
1. donor risk factors:
· use of a donor’s right kidney
· Multiple graft vessels
· prolonged ischemia time
· vascular injuries
· Older age of donors
2. Recipient-related risk factors:
· extremes of age
· peritoneal dialysis
· Perioperative hemodynamic status
3. technical issues: kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium
4. mechanical causes:
· a kink in the renal vein
· compression by hematomas or lymphoceles
· anastomotic stenosis
· extension of an underlying deep venous thrombosis
· compression of the renal vein by the renal artery
5. immunosuppression causes:
· cyclosporine, OKT3 antibody
· high doses of pulsed methyl prednisolone
· anti – thymocyte/antilymphocyte globulin
Clinical manifestations of transplant renal vein thrombosis
· rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock
· Chronic vein thrombosis is usually asymptomatic
· Transplant renal vein thrombosis may be complicated by pulmonary embolism, especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins
Diagnosis of transplant renal vein thrombosis
· High clinical suspicion, trigger the use of duplex ultrasonography
· Conventional gray-scale ultrasonography with color and spectral Doppler is used immediately posttransplant to detect complications early
· thrombus in the renal vein is rarely seen on conventional ultrasonographic imaging, due to deep vascular anastomoses
· Duplex ultrasonography characteristically reveals reversed arterial diastolic flow, a spike-like systolic component, and the renal vein non-visualized
· A finding of isolated reversed or absent diastolic arterial flow is sensitive and not pathognomonic and nonspecific to TRVT
· isolated reversed or absent diastolic arterial flow also can be seen in:
1. severe acute rejection
2. severe acute tubular necrosis
3. hematoma
4. vascular kink
· Although angiography remains the criterion standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity
· nuclear medicine scintigraphy or magnetic resonance angiography, offer excellent alternatives without nephrotoxicity and a greater sensitivity than ultrasonography
· MRA can be done without IV contrast
Management of transplant renal vein thrombosis
· Successful emergency surgical thrombectomy has been reported in the early posttransplant period.
· Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period
· Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT
Preventive strategies
· Careful renal retrieval, renal vein repair, and anastomosis and placement of kidney may help to avoide TRVT
· Adequate training in the techniques of vascular anastomosis and graft recovery
· shortening the long renal vein at the time of transplant
· Ipsilateral transplant is preferred.
· Follow up intravascular volume status in recipient
· duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention
Conclusions
· Patients with high risk for TRVT should be followed closely postoperatively
· multidisciplinary team approach may improve outcome in emergency cases
· The prevention of TRVT is more effective than treatment
What is the level of evidence provided by this article?
Narrative review, evidence 5
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Summary of the article
“Transplant Renal Vein Thrombosis”
This article reviewed the transplant renal vein thrombosis(TRVT), which is a devastating vascular complication that may ultimately end with allograft nephrectomy.
· Reported prevalence of 0.1% to 4.2 % of all transplants.
· The prevalence of TRVT is higher in deceased-donor than in living- donor transplant.
· Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.
The most common vascular complications include:
· Transplant renal artery stenosis.
· Renal graft arterial or venous thrombosis.
· Arterial injury; including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
Causes of transplant renal vein thrombosis
1. Donor-related risk factors:
a) use of a donor’s right kidney; due to:
· the short vein and long artery of the right kidney.
· the right kidney is more difficult to position.
b) Multiple graft vessels.
c) Prolonged ischemia time and vascular injuries.
d) Older age of donors; This is probably because donor hypotension together with ischemia- reperfusion injury may cause the activation of a procoagulant surface from cytokines and the recipient’s immune response with atherosclerotic vessels.
2. Recipient-related risk factors:
a) extremes of age.
b) pretransplant dialysis modality(PD is associated with more graft thrombosis than HD.
c) Perioperative hemodynamic status; hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis.
d) primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
3. Technical issues: ncluding kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
4. Mechanical causes:
· A kink in the renal vein.
· Compression by hematomas or lymphoceles.
· Anastomotic stenosis.
· Extension of an underlying deep venous thrombosis.
· Compression of the renal vein by the renal artery is another risk factor.
5. Immunosuppression-related factors:
· prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti- thymocyte/antilymphocyte globulin.
· Cyclosporine can increase the risk of graft thrombosis due to enhancement of throm- boxane A2 release, thromboplastin generation, platelet aggregation, factor VIII activity, and decreased thrombomodulin activity, hence down-regulation of the protein C anticoagulant pathway.
· Calcineurin inhibitors may also induce hypofibrinolysis by increasing the expression of plasminogen activator inhibitor.
Clinical manifestations of TRVT:
1. The typical clinical presentation:
· rapid onset of oliguria or anuria.
· hematuria with worsening graft function.
· painful swollen graft; which may progress to rupture, hemorrhage, and shock.
2. Chronic vein thrombosis: this is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Diagnosis of TRVT:
1. High clinical suspicion. The clinical diagnosis can be difficult in cases of chronic vein thrombosis, as it is initially asymptomatic.
2. Duplex ultrasonography, it reveals:
a) the reversed or absent diastolic waveform, a sign of extremely high vascular resistance.
· Acute rejection and acute tubular necrosis are the most common differentials for reversed diastolic flow, whereas TRVT remains an uncommon cause of reversed diastolic flow.
b) a spike-like systolic component.
c) non-visualization of the renal vein.
3. Angiography remains the criterion standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
4. Nuclear medicine scintigraphy
5. Magnetic resonance angiography; associated with a risk of NSF in low GFR.
Management of transplant renal vein thrombosis
1. Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy.
· Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
· thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated.
2. The surgical management of vascular complications must include surgical exploration of the allograft.
3. Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT.
Preventive strategies
1. Meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT.
2. Sufficient training in the techniques of vascular anastomosis and graft recovery.
· To shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
· ipsilateral transplant (right to right and left to left) whenever possible.
3. Low-dose aspirin and low-molecular-weight heparin. May be of benefits in high-risk patients:
· Recipients with hypercoagulable profiles.
· Receiver of a kidneys with more than 1 renal artery.
What is the level of evidence provided by this article?
This is a narrative review article.
Level of evidence grade 5.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Please summarise this article
The incidence of transplant renal vein thrombosis is from 0.1 to 4.2%. It usually leads to graft loss. It leads to graft nephrectomy in almost all cases.
Aetiology
Use of a donor’s right kidney
Multiple graft vessels
Vascular injuries
Prolonged ischemia
Older age of donors
Recipient Factors
Extremes of age
Peritoneal dialysis is associated with more graft thrombosis than hemodialysis
Hypotension and dehydration
Technical Issues.
A variety of technical issues have also been implicated as risk factors of TRVT
Kinking of the graft vein
Long vein
Wide disparities in vessel size
Injury to the vascular endothelium during surgical manipulation
Mechanical causes- a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis
Prothrombotic immune suppressants
Diagnosis-
Clinical suspicion
Doppler scan
MRI
Treatment
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period
Emergency surgical thrombectomy has been reported in the early posttransplant period
Combined percutaneous mechanical thrombec – tomy and localized catheter-directed thrombolysis
Conclusion
Patients at high risk for TRVT should be identified and followed postoperatively
A meticulous postoperative protocol is critical to graft and patient survival.
A coordinated multidisciplinary team approach is crucial
The prevention of TRVT by careful attention to predisposing factors
What is the level of evidence provided by this article?
Review article Level V
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Thank you very much Prof
This is a review article with level evidence of 5.
Summary:
Transplant renal vein thrombosis (TRVT) is an early severe complication of renal transplantation. When chronic can be missed because of being asymptomatic, but when acute, it causes severe pain. In either context, the renal function deteriorates, and the chance of surgical solution is ineffective and usually ends with graft loss and obligatory nephrectomy to avoid shock and other serious adverse effects. Thrombolytic therapy or thrombectomy were reported to be of benefit but may not be curative as it is usually late. Thrombolytic therapy carries the disadvantage of massive haemorrhage.
The most appropriate diagnostic tool is a duplex ultrasound. It has the advantage of being non-invasive, with no harmful contrast and quick.
TRVT can be donor, recipient or surgical-related. the use of the right kidney may be a risk due to short vasculature. multiple vessels anastomosis adds a risk. From the recipient’s point of view, extremes of age, and modality of RRT may potentiate the risk. PD is thought to have more risk in relative to HD because of elevated procoagulant factors. Perioperative volume status, hypovolemia and dehydration carry the risk of AKI and thrombosis. Mechanical factors like kinking of renal vein and compression by hematoma or lymphocele, for example, predispose to thrombosis. injury of the endothelium during surgery is also implicated. contralateral implants (transplanting the right kidney to the left iliac fossa e.g.) may potentiate the risk. Other risks are medication related. OKT, cyclosporin, high-pulse steroid and anti-ATG may play a role.
In conclusion, close monitoring and preventive measures are more important because the treatment itself is mostly unsuccessful and ends with graft loss.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Summary of the article;
RVT is rather a critical outcome early occur post operative, and commonly ended by graft loss and nephrectomy.
incidence range between 1-4% of all transplanted kidneys and its more common in deceased donation rather than living donation, and this is attributed to fact that living donation may underwent under favorable condition and less ischemic events.
Causes;
Donor factor;
Recipient factors;
Surgical related;
Immunosuppressants related;
Increased risk with prothrombotic drugs, (CyA, OKT3, High dose pulsed methyl prednisolone, and ATG).
Clinical manifestation;
Diagnosis;
Dopplex US characteristics;
Management;
Conclusion;
Level of evidence;
Level ((V)) article review
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Renal vien thrombosis could be acute or chronic \the acute one usually presented with painful graft and hematuria ,oligoanuric , may progress to rupture, haemorrhage, and shock.
chronic renal thrombosis is usually asymptomatic
Diagnosis is mainly clinical but will need to Doppler of the graft and MRI is the best
managment
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT.
I like your summary and analysis,. You should have typed references.
Ajay
Summary:
Causes of transplant renal vein thrombosis:
Clinical manifestations of transplant renal vein thrombosis:
Diagnosis:
Management:
Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy.
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis have been tried safely and effectively in TRVT.
there are no large randomized controlled studies of sufficient power to assess the relative efficacy of different management approaches.
Preventive strategies:
Level of Evidence:
Level 5 (review article).
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
thank you
Summary:
Transplant Renal Vein Thrombosis
Transplant renal vein thrombosis (TRVT) is a devastating complication causing early graft dysfunction, with reported prevalence of 0.1% to 4.2% of all transplants. TRVT leads to graft loss and nephrectomy in almost all cases. It is more common in deceased donor than in living donor.
Causes of transplant renal vein thrombosis
Donor factors:
a- Donor’s right kidney
due to short vein and long artery of the right kidney. The short vein can be easily compressed by kidney swelling due to ischemic damage, acute tubular necrosis, or urinary obstruction. The kidney is more difficult to position especially if multiple renal arteries are present and the long renal artery can be easily kinked.
b- Multiple graft vessels
c- Prolonged ischemia time which can potentiate thrombogenicity of the endothelium or cause ATN with graft edema that lead decreased perfusion and thrombosis.
d- Vascular injuries
e- Older age of the donor; due to donor hypotension and ischemia reperfusion injury which cause activation of the procoagulant surface from cytokines response and atherosclerotic vessels.
Recipient-related risk factors
a- Extreme of age especially with the atherosclerotic vessels
b- Variation in the vessels sizes between the donor and recipient, especially with pediatric transplantation.
c- Pretransplant dialysis modality; graft thrombosis is more in peritoneal dialysis than hemodialysis.
d- Hypercoagulable states; as antiphospholipid syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
e- Perioperative hemodynamic status: hypotension cause AKI, hypoperfusin and thrombosis.
f- Primary renal disease like membranous nephropathy.
Technical and mechanical issues
a- Kinking of the graft vein,
b- a long vein
c- wide disparities in vessel size
d- injury to the vascular endothelium during surgical manipulation
e- Compression of the vessel by hematoma, or lymphoceles or by renal artery in contralateral transplant procedure, (right kidney into the left iliac fossa and left kidney into the right iliac fossa).
f- Anastomotic stenosis
g- Extension of an underlying DVT
Immunosuppressive drugs
h- Prothrombotic drugs such as cyclosporine, OKT3 antibody, high dose methylprednisolone, and anti –
thymocyte/antilymphocyte globulin.
Clinical manifestations of transplant renal vein thrombosis
Usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
Urologic complications or acute rejection are important differential diagnosis.
Diagnosis of transplant renal vein thrombosis
Duplex ultrasonography, Conventional gray-scale ultrasonography with color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and long-term outcomes of noncomplicated renal transplants.
Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial wave-form positive during systole and negative during diastole), a spike-like systolic component, and nonvisualization of the renal vein.
There are 3 typical shapes of reversed diastolic waveforms: type 1 or “transient” waveform, in which the reversed diastolic waveform returns to baseline before end diastole; type 2 or “plateau” waveform in which a flat reversed flow remains relatively constant throughout diastole; and type 3 or “inverted M” waveform, in which reversed flow
throughout diastole has mid-diastolic deceleration.
Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels.
Angiography remains the golden standard for the diagnosis of renal vascular pathology, it is invasive and associated with significant nephrotoxicity.
Magnetic resonance imaging is now considered a reliable tool for evaluation of renal allografts and the diagnoses of most complications.
Management of transplant renal vein thrombosis
a- Thrombolytic therapy is usually the treatment of choice for TRVT in the late transplant period.
b- surgical thrombectomy in the early post-transplant period.
Preventive strategies
Technical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, anastomosis and placement of kidneys may hold considerable importance in the avoidance of TRVT.
It is narrative review level 5
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Post-transplant vascular complications occur in -% of recipients, TRVT is one of the major complications that can lead to graft loss. It is more common in deceased donor transplants due to the associated ischemic injury.
Causes of TRVT:
Donor related risk factors:
Elderly donors, using donor’s right kidney, multiple graft vessels, prolonged ischemia times and vascular injuries.
Recipient related risk factors:
Extremes of age, peritoneal dialysis, hypercoagulable state, hypotension and dehydration preoperatively and primary renal disease as membranous GN.
Technical issues:
Kinking of graft vein, compression by hematoma or lymphocele, injury to vascular endothelium, anastomotic stenosis and extension of underlying DVT.
Immunosuppressive therapy with prothrombotic effect as cyclosporine, pulse methyl prednisolone and ATG.
Clinical manifestations:
Usually asymptomatic, typically present with oliguria, hematuria, deteriorating graft function and painful swollen graft that may progress to rupture and hemorrhage.
Diagnosis:
Requires high suspicion
Duplex ultrasonography:
Used early post transplant to detect early complications, calculate resistive index and pulsatile index.
Safe, noninvasive with no exposure to radiation or contrast media.
Reveals reversed arterial diastolic flow, spike like systolic component and non visualization of renal vein, with 3 typical shapes of reversed diastolic waveforms, “transient”, “plateau” and “inverted M”.
Isolated reversed or absent diastolic arterial flow is sensitive but not pathognomonic to TRVT.
Diagnosis is affected by patient’s body habitus, operator skills and availability of acoustic window.
CT angiography:
Provide definite diagnosis but invasive, use nephrotoxic contrast
Nuclear medicine scintigraphy and MR angiography:
More sensitive than U/S, no nephrotoxic agents used.
MR angiography with recent modalities used without contrast and screen for vascular complications.
limited use due to higher cost, long examination time and lack portability.
Management:
Thrombolytic therapy:
Used late post transplant
May cause life threatening hemorrhage
Surgical thrombectomy:
More successful early posttransplant, detect the cause and can correct the technical complications.
Associated with risk of anesthesia and post operative infection.
Combined percutaneous mechanical thrombectomy and localized catheter directed thrombolysis were tried safely and effectively.
Success rate of all interventions is variable and long term outcome is not determined.
Preventive strategies:
Meticulous surgical techniques, sufficient training in techniques of vascular anastomosis and graft recovery
Shortening of long renal vein to avoid kinking
Ipsilateral transplant whenever possible
Avoiding hypovolemia and hypotension.
Monitoring with duplex ultrasonography during early period post transplant.
Low dose aspirin and LMWH in high risk patients.
Level of evidence: 5 (narrative review)
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
· Introduction:
– The most common vascular complications after kidney transplantation include transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
– Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants. Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases. The prevalence of TRVT is higher in deceased-donor than in living donor transplant. This may be because living-donor transplant procedures are usually done under more favorable conditions and are not usually subjected to ischemic injury
· Causes :
– often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
>> donor risk factors :
– use of a donor’s right kidney is associated with the development of renal graft thrombosis due to the short vein and long artery of the right kidney. The short renal vein can be easily compressed postoperatively by the kidney swelling due to ischemic damage, acute tubular necrosis, or urinary obstruction. The right kidney is more difficult to position, especially if multiple renal arteries are present and the long artery can be easily kinked.
– Multiple graft vessels have been also implicated in renal graft thrombosis in some studies, although refuted in others. In addition, prolonged ischemia time and vascular injuries have been found to be donor risk factors for renal graft thrombosis.
– The prolonged ischemia time could potentiate thrombogenicity of the endothelium, or a resulting acute tubular necrosis with graft edema could lead to decreased perfusion and thrombosis.
– Older age of donors is associated with an in – creased risk of graft thrombosis.This is probably because donor hypotension together with ischemiareperfusion injury may cause the activation of a procoagulant surface from cytokines and the recipient’s immune response with atherosclerotic vessels.
>>Recipient-related risk factors:
– extremes of age which may call for more complex surgical procedures, especially with atherosclerotic vessels predisposing to a higher incidence of thrombosis, and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures.
– pretransplant dialysis modality in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
– Perioperative hemodynamic status in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis, and primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
>>technical issues :
– kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
– a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
– compression of the renal vein by the renal artery is another risk factor, especially in contralateral transplant procedures (right kidney into the left iliac fossa and left kidney into the right iliac fossa).
>>immunosuppression:
– TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti – thymocyte/antilymphocyte globulin.
· Clinical manifestations:
– The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
– Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
– Clinical diagnosis may be easy in cases of acute renal vein thrombosis, although not specific, with diagnosis perhaps confused with the occurrence of a urologic complication or acute rejection, the 2 most frequent complications during the early post – operative period. Transplant renal vein thrombosis may be complicated by pulmonary embolism, especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins
· Diagnosis :
– usually based on a highly suspicious clinical presentation, triggering assessment using duplex ultrasonography.
– The clinical diagnosis can be difficult in cases of chronic vein thrombosis, as it is initially asymptomatic.
– Conventional gray-scale ultrasonography with color and spectral Doppler is used immediately posttransplant for early detection of complications and evaluation of the renal allograft; it also allows calculation of resistive index and pulsatile index, which may predict early and long-term outcomes of noncomplicated renal transplants . It is noninvasive and is an easily available tool that avoids use of ionizing radiation and iodinated contrast media.
– Duplex ultrasonography characteristically reveals reversed arterial diastolic flow (ie, the arterial wave – form positive during systole and negative during diastole), a spike-like systolic component, and nonvisualization of the renal vein . Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessels. This high vascular resistance indicates graft dysfunction and correlates with increased risk of graft loss. A finding of isolated reversed or absent diastolic arterial flow is sensitive and not pathognomonic and nonspecific to TRVT and may also be seen in an array of causes,such as severe acute rejection, severe acute tubular necrosis, hematoma, and vascular kink. Acute rejection and acute tubular necrosis are the most common causes of reversed diastolic flow, whereas TRVT remains an uncommon cause of reversed diastolic flow.
– MRA without gadolinium contrast is an alternative to angiography .
· Management :
– Successful emergency surgical thrombectomy has been reported in the early posttransplant period. Operative interventions can facilitate better evaluation of the cause of thrombosis and can allow for the correction of technical complications and without too many technical difficulties caused by fibrosis.
– Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period
>>Preventive strategies :
– meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable importance in avoidance of TRVT. Sufficient training in the techniques of vascular anastomosis and graft recovery is critical, to avoid multiple attempts during the operation and the subsequent iatrogenic vascular trauma.
– A long renal vein is considered a risk factor of , the authors here recommend routinely shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis. also prefer ipsilateral transplant (right to right and left to left) whenever possible and also in cases of short renal vessels (eg, living-donor transplant procedures) to avoid compression of the renal vein by the renal artery.
– Attention to intravascular volume status in patients undergoing renal transplant is recommended. Transesophageal Doppler has been used to monitor the fluid balance during the procedure because it has been more accurate than measurement of central venous pressure.
– Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period followed by timely intervention may result in successful salvage of a renal allograft
– Some protocols include an hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels.This proactive surveillance approach posttransplant may lead to an early diagnosis, thus allowing salvage of the renal allograft.
– Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients, especially in recipients with hypercoagulable profiles or those who received kidneys with more than 1 renal artery.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Please summarise this article
Introduction:
Post operative vascular complications in kidney transplantation are major challenges, occur in 1-10% of case and they are:
Transplant renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
Transplant renal vein thrombosis (TRVT) has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant, with a prevalence of 0.1% to 4.2 % of all transplants.
Causes of transplant renal vein thrombosis:
Donor related: donor’s right kidney is associated with the development of renal graft thrombosis, Multiple graft vessels, prolonged ischemia time, and Older age of donors.
Recipient related: older age recipients, variations in vessel sizes between the donor and recipient, pretransplant dialysis modality (peritoneal D > HD), history of thrombophilia, antiphosphlipid antibody, primary memebranous nephropathy, and preoperative hemodynamic status.
Perioperative mechanical related: renal vein kinking or compression due to hematoma or lymphocele, extension of underlying DVT, compression of the renal vein by the renal artery especially in contralateral transplant procedures, use of cyclosporine, ATG, and OKT3 antibodies.
Cyclopsorin use related is due to enhancement of thromboxane A2 release, and/or induce hypofibrinolysis.
Clinical manifestations of transplant renal vein thrombosis:
Rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful graft swelling.
Thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus, may be complicated by pulmonary embolism.
Differential diagnosis are urological complication and acute rejection.
Diagnosis of transplant renal vein thrombosis:
Ultrasound + duplex ultrasound: suggested when reversed or absent arterial diastolic flow ensue, a spike-like systolic component, and nonvisualization of the renal vein, and very high resistive index.
Venography/angiography the gold standard but contrast induced nephropathy of concern.
Medical scintigraphy and MRI are used.
Management of transplant renal vein thrombosis:
As prevention is better than cure preventive measures for decreasing the above mentioned causes of TRVT is a must.
Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients.
Thrombolytics and thrombectomy is the treatment modalities use early after diagnosis.
Unfortunately the end result is graft nephrectomy either due to late diagnosis or failed thrombolytics or thrombectomy.
Conclusion:
Knowing the risk factors of TRVT, and doing all preventing measures, expertized surgeon, and use of low dose aspirin and low molecular weight heparin early post-transplant can decrease the incidence.
What is the level of evidence provided by this article?
Level of evidence V
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Introduction:
Ø Renal transplant is the best option for the treatment of patients with end-stage renal disease
Ø postoperative vascular complications are, occurring in 1% to 10% of transplanted patients
Ø The most common vascular complications :
1- transplant renal artery stenosis,
2- renal graft arterial or venous thrombosis
3- arterial injury, including
I. arteriovenous fistulas,
I. intrarenal pseudoaneurysms,
II. arterial dissection,
III. arterial-calyceal fistulas
Transplant renal vein thrombosis:
The leading causes of early graft dysfunction after renal transplant, with a reported prevalence of 0.1% to 4.2 % of all transplants.
The prevalence of TRVT is higher in deceased-donor than in living donor transplants.
Causes:
1-donor factors,
2-recipient factors,
3-technical issues during transplant surgery
Donor risk factors:
1-use of a donor’s right kidney.
2-Multiple graft vessels.
3-vascular injuries
4-prolonged ischemia time
5-Older age of donors
Recipient-related risk factors:
1-extremes of age,
2-pretransplant dialysis modality peritoneal dialysis is associated with more graft thrombosis than hemodialysis
3-Peri operative hemodynamic status
4-mechanical causes: Kinking of the grafted vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation
5-administration of prothrombotic drugs such as cyclosporine, OKT3 antibody
Clinical manifestations of transplant renal vein thrombosis:
Ø The typical clinical presentation is usually the rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft
Chronic vein thrombosis is generally asymptomatic.
Diagnosis of transplant renal vein thrombosis:
clinical presentation
duplex ultrasonography
Management of transplant renal vein thrombosis
Two strategies are available for treating venous thrombosis of renal allograft: thrombolytic therapy and surgical thrombectomy
Preventive strategies:
1-meticulous surgical techniques
2-Sufficient training in the methods of vascular anastomosis.
3-Attention to intravascular volume status in patients undergoing renal transplant
4-Transesophageal Doppler has been used to monitor the fluid balance during the procedure
5-Meticulous clinical assessment and duplex ultrasonography monitoring during the early posttransplant period
6-Low-dose aspirin and low-molecular-weight heparin
Conclusions:
The prevention of TRVT by identify the predisposing factors, including technical
details of surgical procedures, donor and recipient risk factors ,use of heparine and asprine as prophylactic.
level 5.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
club 6, renal vein thrombosis after KT
Summary:
· Vascular complications occur in 1-10% of renal transplant cases.
· They include renal artery stenosis, renal graft arterial or venous thrombosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dis – section, and arterial-calyceal fistulas.
· RVT has detrimental effect on the graft function and causes early graft loss.
· Risk factors for RVT:
o Donor related factors: the donated right kidney with short vein and long artery, especially with multiple renal arteries, prolonged ischemia time that causes the endothelium to be more antigenic, older age of the donors.
o Recipient related factors: older age with atherosclerosis, discrepancy in size of renal vessels between the donor and the recipient especially in pediatric kidney transplantation, procoagulant conditions as antiphospholipid syndrome and inherited coagulopathy, perioperative hypotension that precipitate ATN and graft hypoperfusion and thrombosis, original kidney disease as membranous nephropathy (increased risk of thrombosis), need for dialysis prior to transplantation (especially PD due to accumulation of procoagulant factors than in HD).
o Surgical technique related factors: kinking of the vein or injury to the endothelium.
o Kinking of renal vein or compression of the allograft by hematoma or lymphocele are the common risk factors. Compression of the renal vein by the renal artery is another risk factor, especially in contralateral transplant procedures (right kidney into the left iliac fossa and vice versa).
o Immunosuppression used: high dose steroids, IVIG, OKT3 or ATG. in addition, CNI especially cyclosporine has thrombogenic activity.
· Clinical presentation;
o Acute graft dysfunction (oligo-anuria, hematuria) that is none specific and similar to that of acute rejection and urological complications that are commonly presented early post-transplant period.
o Tender graft that may rupture causing shock.
o consumption thrombocytopenia can be observed few hours after RVT.
o Extension of lower limb DVT usually presented with concomitant pulmonary embolism.
· Diagnosis:
· Abdominal US with color duplex (safe, cheap, available, avoid ionizing radiation and use of nephrotoxic contrast).
o As regard grey scale US: the renal vein is deep in the recipient’s pelvis, thrombus in the renal vein is rarely seen.
o RVT is diagnosed by color duplex by:
· None visualized renal vein.
· Presence of reversed diastolic flow (the wave become negative in diastole below the zero line),
· Reversed or absent diastolic flow is a sign of extremely high vascular resistance in small intrarenal or large extrarenal vessel which indicates graft dysfunction and is associated with higher incidence of graft loss. however, it is not pathognomonic for RVT.
o Differential diagnosis of reversed diastolic flow early post-transplant (30 days): severe acute rejection, severe ATN, hematoma, and vascular kink. AR and ATN are the most common causes of reversed diastolic flow, whereas TRVT is an uncommon cause.
o Differential diagnosis of reversed diastolic flow late post-transplant ( >30 days): rejection, glomerulosclerosis, low cardiac output).
· Angiography remains the gold standard for the diagnosis of renal vascular pathology, but it is invasive and has significant nephrotoxicity. Hence, nuclear medicine scintigraphy or MRA, is an excellent alternative with better sensitivity than US.
· MRA with gadolinium-based contrast agents is associated with risk of nephrogenic systemic fibrosis in patients with lower GFR. However, imaging modalities have been developed to view the vessels without intravenous contrast. the cost, unavailability, need for anesthesia in children and inaccessibility in critically ill patients are still limitations of MRI.
· Management of RVT:
o Thrombolytic therapy and surgical thrombectomy
o Surgical exploration and graft nephrectomy.
o Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis can be used in none responsive cases.
o Thrombolytic therapy is best in late presentation, has risk of thrombus mobilization and hemorrhage.
o Surgical thrombectomy has risk of anesthesia and infections.
· Prevention is better than cure, due to poor outcome of RVT and inferior outcome of graft salvage procedures, so care about surgical techniques regarding renal retrieval, renal vein repair, and anastomosis are essential to prevent RVT.
o Training on surgical techniques and vascular anastomosis to minimize repeated trial and crashing of vessels, shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis and preference of ipsilateral transplant (right to right and left to left) to avoid renal vein compression by renal artery.
o Optimization of intravascular volume through close monitoring by Transesophageal Doppler (more accurate than measurement of central venous pressure) to prevent graft hypoperfusion.
o Close monitoring of the patient (vital data and urine output), laboratory parametrs of the graft function (creatinine and electrolytes) and duplex (for adequate perfusion of the graft) is essential for early detection and management of any complications.
o Antiplatelet and LMWH can be used for prophylaxis in high risk patients (hypercoaguable state and multiple renal arteries).
· Level of evidence: narrative review (level V).
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
Introduction;
—————————-
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after renal transplant . Transplant renal vein thrombosis events lead to graft loss and nephrectomy in almost all cases.
The prevalence;
—————————–
a reported prevalence of 0.1% to 4.2 % of all transplants. The prevalence of TRVT is higher in deceased-donor than in living- donor transplant.
Causes of transplant renal vein thrombosis;
—————————————————
The pathogenesis of this devastating complication is often multifactorial and includes donor factors, recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
Donor risk factors ;
————————
1-use of a donor’s right kidney is associated with the development of renal graft thrombosis, due to the short vein and long artery of the right kidney.
2-The right kidney is more difficult to position, especially if multiple renal arteries are present and the long artery can be easily kinked.
3-Multiple graft vessels have been also implicated in renal graft thrombosis in some studies, although refuted in others.
4-Prolonged ischemia time and vascular injuries have been found to be donor risk factors for renal graft thrombosis.
5- Older age of donors is associated with an in- creased risk of graft thrombosis.
Recipient-related risk factors;
————————————
1-Extremes of age, which may call for more complex surgical procedures, especially with atherosclerotic vessels predisposing to a higher incidence of thrombosis, and variations in vessel sizes between the donor and recipient, especially with pediatric transplant procedures.
2- Peritoneal dialysis is associated with more graft thrombosis than hemodialysis, due to elevated plasma procoagulant factors, hypercoagulable states, including antiphospholipid antibody syndrome, antithrombin deficiency, mutation of factor V Leiden, and the prothrombin gene.
3-Perioperative hemodynamic status, in which hypotension and dehydration could predispose to acute kidney injury, hypoperfusion, and thrombosis.
4- Primary renal disease such as membranous nephropathy have also been identified as risk factors for venous graft thrombosis.
Operative factors.
—————————
1-A variety of technical issues have also been implicated as risk factors of TRVT, including; kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium during surgical manipulation.
2-The following mechanical causes are considered the most common causes of TRVT: a kink in the renal vein, compression by hematomas or lymphoceles, anastomotic stenosis, and extension of an underlying deep venous thrombosis.
Immunosuppression factors ;
——————————————
TRVT can also be triggered by administration of prothrombotic drugs such as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and anti-
thymocyte/antilymphocyte globulin.
Clinical manifestations of transplant renal vein thrombosis;
——————————————————————————————————-
The clinical manifestations of acute renal vein thrombosis are nonspecific and are not dissimilar to the features of urine leak, urinary obstruction, or severe acute rejection.
1-The typical clinical presentation is usually rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
2-Chronic vein thrombosis is usually asymptomatic. However, thrombocytopenia may occur after a few hours as a consequence of platelet sequestration in the thrombus.
3-Transplant renal vein thrombosis may be complicated by pulmonary embolism,
especially when it is associated with and related to the extension of deep vein thrombosis of lower limb veins.
Diagnosis of transplant renal vein thrombosis;
———————————————————————
The diagnosis of transplant renal vein thrombosis depends on a high index of clinical suspicion and duplex ultrasonographic scans. Although venography remains the criterion standard, this procedure is invasive and nephrotoxic, due to use of ionizing contrast agents and also due to exposure to ionizing radiation.
Management of transplant renal vein thrombosis;
—————————————————————————-
1-Thrombolytic therapy .
Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.Thrombolytic treatment can cause life-threatening hemorrhage, especially in the perioperative period, and may lead to clot migration when lytic therapy is initiated.
2-Surgical thrombectomy;
Surgical thrombectomy has risks associated with anesthesia and postoperative infection in an immunosuppressed state.
3- Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis;
Have been tried safely and effectively in TRVT, notably after the second week after transplant with subacute or chronic TRVT and also in acute TRVT when prolonged thrombolysis has failed or is contraindicated .
The success rate for these interventions is variable among different studies, which are either case or cohort studies. Unfortunately, there are no large randomized controlled studies of sufficient power to assess the relative efficacy of different management approaches.
Preventive strategies;
—————————————-
1-Technical issues seem to play a major role; therefore, meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis and placement of kidney may hold considerable impor tance in avoidance of TRVT.
2-Sufficient training in thetechniques of vascular anastomosis and graft recovery is critical, to avoid multiple attempts during the operation and the subsequent iatrogenic vascular trauma.
3- Shorten the long renal vein at the time of transplant to prevent kinking and subsequent thrombosis.
4- Uses the ipsilateral transplant (right to right and left to left) whenever possible and also in cases of short renal vessels to avoid compression of the renal vein by the renal artery.
5- Attention to intravascular volume status in patients undergoing renal transplant is recommended.
6- Uses strict protocols for postoperative monitoring of the renal allograft to allow prompt, early diagnosis of any complications. Such protocols include an hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels.
7- Low-dose aspirin and low-molecular-weight heparin may also have benefits in preventing renal vein thrombosis in high-risk patients, especially in recipients with hypercoagulable profiles or those who received kidneys with more than 1 renal artery.
What is the level of evidence provided by this article?
—————————————————————————–
Level V
Hi Dr Ishag,
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late. Your headings and sub-headings should be in bold or underline. That will make it easy to read.
It is level 5 evidence.
Ajay
Transplant renal vein thrombosis (TRVT) of an allograft has a dramatic clinical presentation and is one of the main causes of early graft dysfunction after RT.
The prevalence of TRVT is 0.1% to 4.2 %, and it is higher in DD than in DD transplants.
Causes of transplant renal vein thrombosis
Donor risk factors:
The use of the donor’s right kidney due to the short vein and long artery of the right kidney.
Multiple graft vessels.
Prolonged ischemia time.
Vascular injuries.
Older age.
Recipient-related risk factors
Extremes of age>> more complex surgical procedures.
Atherosclerotic vessels.
Variations in vessel sizes between the donor and recipient.
Dialysis modality: PD carries a higher risk.
Hemodynamic status, hypotension and dehydration.
Primary renal disease such as MNP.
Technical issues:
Kinking or compression of the graft vein, a long vein.
Wide disparities in vessel size.
Injury during surgical manipulation.
Immunosuppression:
Prothrombotic drugs such as CsA, OKT3 antibody, IVMP, AtG
Clinical manifestations:
Acute RVT: Rapid onset of oliguria or anuria, hematuria with worsening graft function, and a painful swollen graft, which may progress to rupture, hemorrhage, and shock.
Chronic RVT; usually asymptomatic, thrombocytopenia occurs.
Diagnosis:
Duplex ultrasonography
noninvasive and readily available.
No ionizing radiation and iodinated contrast media.
Allows calculation of resistive index and pulsatile index, which may predict graft outcome.
Characteristically:
Reversed arterial diastolic flow: retrograde blood flow occurred at any time point during the diastole
Sign of vascular resistance.
sensitive and not pathognomonic and nonspecific to TRVT, also seen in rejection, ANT, hematoma, and kinking.
3 typical shapes of reversed diastolic waveforms
type 1 or “transient”: the reversed diastolic waveform returns to baseline before end diastole
type 2 or “plateau”: a flat reversed flow remains relatively constant throughout diastole. Carries a higher rate of graft
loss.
type 3 or “inverted M”; reversed flow throughout diastole has mid-diastolic deceleration.
Angiography is the gold standard for the diagnosis
Nuclear medicine scintigraphy
Magnetic resonance angiography is more sensitive than US. It has some limitations as it can’t be used in pacemakers, it costs, a long time, and the risk of NSF.
Management of TRVT:
Emergency surgical thrombectomy:
In the early transplant period.
Evaluation of the cause of thrombosis
Correction of technical complications
Thrombolytic therapy:
Late transplant period.
Risks; life-threatening hemorrhage, clot migration.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis
Preventive strategies
Meticulous surgical techniques regarding renal retrieval, renal vein repair, and anastomosis.
Shorten the long renal vein at the time of transplant to prevent kinking
Ipsilateral transplant whenever possible
Careful assessment of volume status.
Duplex US monitoring during the early posttransplant period, followed by the timely intervention
Low-dose aspirin and LMWH in a specific population.
Level of evidence 5 narrative review
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
I agree it is level 5 evidence.
Ajay
Introduction
The most common vascular complications after transplantation include transplant renal
artery stenosis, renal graft arterial or venous throm –
bosis, and arterial injury, as AV fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
Transplant renal vein thrombosis (TRVT) is the main cause of early graft dysfunction after renal transplant.
TRVT is more commonly associated with kidneys from deceased donors rather than grafts from living donors due to the exposure to ischemic injury.
Causes of transplant renal vein thrombosis
· Donor factors
Donor’s right kidney is associated with renal graft thrombosis attributed to the short vein which is easily compressed by kidney swelling and long artery of the right kidney which is easily kinked.
Multiple graft vessels were implicated in renal graft thrombosis.
Prolonged ischemia time and vascular injuries can be superadded factors.
Old donor age is accompanied with activation of a
procoagulant surface from cytokines and the
recipient’s immune response with atherosclerotic
vessels.
· Recipient factors
Include age extremes with variation in donor and recipient vessel size
Pretransplant dialysis modality because peritoneal dialysis is more liable to graft thrombosis rather than hemodialysis due to the hypercoagulable status.
Perioperative hypotension and primary renal disease.
· Technical issues during transplant
As kinking of the graft vein, a long vein, wide disparities in vessel size, and injury to the vascular endothelium.
Compression by hematomas or lymphoceles,
Anastomotic stenosis, and extension of DVT.
Renal artery can compress the vein in contralateral procedures.
· Surgical factors
· Immunosuppression
By prothrombotic drugs as cyclosporine, OKT3 antibody, high doses of pulsed methyl prednisolone, and antithymocyte/antilymphocyte globulin.
Clinical picture
Rapid onset of oliguria or anuria, hematuria with graft dysfunction, and painful graft that can rupture, causing haemorrhage, and shock.
Chronic vein thrombosis is asymptomatic but thrombocytopenia can occur.
It can be complicated with pulmonary embolism particularly if associated with DVT.
Diagnosis
By clinical suspicion , duplex ultrasonography to evaluate the renal allograft, and calculation of resistive index and pulsatile index to predict short and long term outcomes.
Renal vein thrombosis is rarely seen by conventional ultrasonography.
Duplex ultrasonography shows reversed or absent arterial diastolic flow which is a sign of extremely high
vascular resistance in small intrarenal or large
extrarenal vessels.
Reversed diastolic waveforms are either transient , plateau or M shaped.
Isolated reversed or absent diastolic arterial flow is sensitive but not pathognomonic to TRVT and can be seen in severe acute rejection, severe ATN , hematoma, and vascular kink.
Angiography is invasive and nephrotoxic.
Magnetic resonance angiography is a reliable method to screen for vascular abnormalities in renal allografts.
IV gadolinium can be eliminated to avoid nephrogenic systemic fibrosis in cases with low GFR.
MRI cannot be used for cases with pacemakers and it is expensive with long exam time.
Management
Thrombolytic therapy , surgical thrombectomy.
Thrombolytic therapy can be done in the late transplant period , it is the treatment of choice can be complicated with haemorrhage while
Surgical thrombectomy usually done in the early transplant period , it carries risks as that of anesthesia ,infection.
Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis can be done after the second week of transplant with subacute or chronic TRVT and in acute TRVT.
when prolonged thrombolysis has failed.
Prevention
Meticulous surgical techniques for renal
retrieval, renal vein repair, and anastomosis and
placement of kidney are crucial in avoidance of TRVT.
As shortening long renal vein at the time of transplant to prevent kinking and subsequent thrombosis and ipsilateral transplant is preferred .
Intravascular volume monitoring in renal transplant by transoesophageal doppler.
Duplex ultrasonography monitoring during the
early posttransplant period and follow up.
Strict postoperative monitoring as hourly measurement of urine output, daily duplex ultrasonography scanning, and daily measurements of serum creatinine and electrolyte levels.
Low-dose aspirin and low-molecular-weight
heparin can help prevent renal vein thrombosis in high-risk patients.
Conclusion
Recipients with high risk for TRVT need postoperative follow up to allow early diagnosis and prophylactic measures.
MDT is needed to improve graft outcome.
Prevention of TRVT is much better than treatment to salvage the graft.
– Level of evidence 5
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
I agree it is level 5 evidence.
Ajay
SUMMARY
Introduction
Kidney transplantation is the best form of renal replacement therapy, but it also comes with post-transplant vascular complications and top on this list is transplant renal vein thrombosis with prevalence of 0.2% -4.2% and has been reported to be higher in diseased donor than living donor. It’s a complication with very high rate of graft lost even if detected early.
Causes of TRVT
A) Donor risk factor
B) Recipient related risk factor
C) Mechanical causes
D) Immunosuppressive causes
Clinical manifestation
Diagnosis of TRVT
Treatment of TRVT
Prevention of TRVT
Conclusion
Transplant vein thrombosis is among most feared complication because of its lethal outcome graft survival, hence identification of risk factors or causes among donor, recipient, and surgical methods is important in preventing the incidence of TRVT. Moreso, early treatment may be of help in salvaging the graft from complete rejection.
Level of evidence is 5
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay
TRVT
This is post-transplant complications can be happened early with 0.1-4% incidence rate from all transplant, usually diagnosed late as it is clinically similar to urinary obstruction and urine like and even acute rejection, and its diagnosis depends on the clinical suspicion, usually has bad prognosis ends by graft nephrectomy.
Causes of TRVT:
1- Donor factors like old age donor, deceased donor, right kidney as a graft as she has short vein and long artery , also kidney of multiple vessels, prolonged ischemic time, hypotension and ischemia in the donor side can cause ATN and edema inside the graft which predispose to thrombosis.
2- Recipient factors old age recipient due to atherosclerotic vessels , pediatric recipient due to small size vessels, antiphospholipid syndrome, and procoagulant medical condition , primary kidney disease like membranous nephropathy, also modality of dialysis as peritoneal dialysis is associated with circulating pro coagulant factors.
3- Technique related factors vessel injury during anastomosis or nephrectomy, small size vessels or discrepancy in the vessel size, kinked vein.
4- mechanical causes (most common causes of TRVT)
a- kink in the renal vein
b- compression by hematomas or lymphoceles
c- anastomotic stenosis
d- extension of an underlying deep venous thrombosis
5- immunosuppressive medication related factors: CNI, ATG, OKT3, high dose pulse methylprednisolone all are procoagulant or prothrombotic drugs.
Clinically can be manifested by oliguria, anuria, hematuria, elevated renal function, painful graft in acute RVT but the chronic one is asymptomatic.
Diagnosed by:
Conventional gray-scale ultrasonography with color and spectral Doppler which reveals reversed arterial diastolic flow but this picture is nonspecific for RVT and can be seen in cases of ATN, severe acute rejection, hematoma and kinked vessel, so clinical suspicion is very important in diagnosis.
Magnetic resonance imaging MRA is a good tool to evaluate the graft, so imaging without contrast is advised to avoid nephrogenic systemic sclerosis with gadolinium in the patient with low GFR.
How to manage RVT:
1- surgical approach thrombectomy especially in early period post transplant
2- medical approach with thrombolytic therapy especially in the late period
3- Combined percutaneous mechanical thrombectomy and localized catheter-directed thrombolysis
level of evidence 4
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
I agree it is level 5 evidence, not 4 as per Oxford description of level of evidence.
Ajay
Introduction
*postoperative vascular complications are major challenges, occurring in 1% to 10% of transplanted patients
*The most common vascular complications include transplant renal artery stenosis, renal graft arterial or venous throm -bosis, and arterial injury, including arteriovenous fistulas, intrarenal pseudoaneurysms, arterial dissection, and arterial-calyceal fistulas.
*Transplant renal vein thrombosis (TRVT) is one of the main causes of early graft dysfunction after renal transplant
Causes of transplant renal vein thrombosis
*multifactorial
includes donor factors,recipient factors, technical issues during transplant surgery (operative factors), and immunosuppression.
*donor’s right kidney is associated with the devel –
opment of renal graft thrombosis,due to the short vein and long artery of the right kidney
* Multiple graft vessels
*prolonged ischemia time and vascular injuries
*Older age of donors
*Recipient-related risk factors include extremes of age,
pretransplant dialysis modality(in which peritoneal dialysis is associated with more graft thrombosis than hemodialysis) And Perioperative hemodynamic status.
*mechanical causes are considered
the most common causes of TRVT: a kink in the renal
vein, compression by hematomas or lymphoceles,
anastomotic stenosis, and extension of an underlying
deep venous thrombosis.
Clinical manifestations of transplant renal vein
thrombosis
The typical clinical presentation is usually rapid
onset of oliguria or anuria, hematuria with wor –
sening graft function, and a painful swollen graft,
which may progress to rupture, hemorrhage, and
shock
Diagnosis of transplant renal vein thrombosis
*based on a highly suspicious clinical presentation,
triggering assessment using duplex ultrasonography
*Duplex ultrasonography characteristically reveals
reversed arterial diastolic flow :
There are 3 typical shapes of reversed diastolic waveforms: -type 1 or “transient” waveform in which the reversed diastolic waveform returns to baseline before end
diastole
-type 2 or “plateau” waveform in which a flat reversed flow remains relatively constant throughout diastole
-type 3 inverted M” waveform in which reversed flow throughout diastole has mid-diastolic deceleration.
Acute rejection and acute tubular
necrosis are the most common causes of reversed
diastolic flow, whereas TRVT remains an uncommon
cause of reversed diastolic flow.
*Magnetic reso nance angiography is increasingly used to screen for vascular abnormalities in renal allografts
Limitations of magnetic resonance imaging in –
clude the inability to image patients with pace makers,
greater cost, lack of portability, and prolonged
examination time, which is not suited to these
critically ill patients.
Management of transplant renal vein thrombosis
*Two strategies are available thrombolytic therapy and surgical thrombectomy.
*Thrombolytic therapy is usually the treatment of choice for TRVT occurring in the late transplant period.
Preventive strategies
*Sufficient training in the techniques of vascular anastomosis and graft recovery is critical, to avoid multiple attempts during the operation and the subsequent iatrogenic vascular
*shorten the long renal vein at the time of transplant to
prevent kinking and subsequent thrombosis.
*ipsilateral transplant
*avoid compression of the renal vein by the renal artery
* clinical assessmentand duplex ultrasonography monitoring during the early posttransplant period
*Low-dose aspirin and low-molecular-weight heparin may also have benefits.
I like your summary and analysis.However, I have never seen success of thrombectomy or thrombolytic therapy in a patient with RVT. By the time, RVT is diagnosed, it is too late.
It is level 5 evidence.
Ajay