The impact factor is calculated by dividing the number of citations in the JCR year by the total number of articles published in the two previous years
The impact factor is just a measure of the number of citations a journal gets over a time period. It is not based on any peer review. The article from the journal can be cited in non-peer review journals, books, thesis, presentations. New journals, because of the time period of two years, don’t have an impact factor and may be considered not to be very relevant in that particular field
The Impact Factor is calculated by dividing the number of citations in the journal citation report per year by the total number of articles published in the two previous years.
The ratio of number of citations in a particular journal over the previous two years to the number of publications in the journal over the same period of time
-Some journals may not have a high impact factor which may lead to their underestimation and yet the are still a good journals
The journal Impact Factor is the average number of times articles from the journal published in the past two years have been cited in the Journal citation report year. The Impact Factor is calculated by dividing the number of citations in the Journal citation report year by the total number of articles published in the two previous years. Journals may be biased toward positive results because negative results are less likely to be cited and can thus lower a journal’s impact factor
Impact factor of a journal = Total number of times its articales were cited during the two previous years ÷ Total number of citable articales in the journal during those two years.
Calculation is based on a two-year period and involves number of times articles were cited divided by the number of citable articles.
For Example: Calculation of 2021 IF of journal
A=the number of times articles [published in 2019 and 2020] were cited by indexed journals during 2021
B=Total number of citable articles published by journal in 2019 and 2020
A/B=2021 IF of journal
It is used to evaluate the importance or rank of a journal by calculating the times its articles are cited.
What is the bias involved in relying on the impact factor(IF) to assess journals?
Self-Citation Bias: If self-citations are used in the introduction or discussion, to stress one’s own conviction, this could lead to bias.
The probability of being cited seems more associated with positive study outcomes (supportive Publications), the authority of its authors and the journal in which it is published.
Reviews would have a higher probability of being cited than original Research studies. Also, original research studies will be less cited once they have been taken up in a (systematic) review.
Journals publishing many review articles usually have high Impact Factors, because review articles usually have a higher average rate of citation than empirical studies/original papers.
Higher sample size study is likely to be more cited than small sample size irrespective of quality of study design.
Journals with large number of articles published are more likely to contain highly cited articles and high IF than journals with small numbers of articles published.
Quality of study is not correlated with citation. citation does not reflect the scientific merit of the cited work and articles are cited for various reasons
Two years duration is less for assessing how important is the journal. Articles cited within two years after publication contribute to the impact factor although many landmark papers achieve their maximal scientific impact outside of this timeframe.
Differences in citation patterns among disciplines are not considered, which makes it impossible to compare journals across disciplines.
the impact factor of a journal is calculated by dividing the number of current year citations to the source items published in that journal during the previous two years.
Limitations and bias:
All citations are weighted equally regardless of the prestige of the citing journal.
Differences in citation patterns among disciplines are not considered
The context of citations is not considered
Only articles that are cited within two years after publication contribute to the impact factor
Citations made in journals not recorded in the Web of Science database do not contribute to impact factor calculations
Citations are gathered from journal articles only, and not from books, book chapters, or conference proceedings.
the impact factor is calculated by dividing the number of citations in the journal citation report per year by the total number of articles published in the two last years.
IF is calculated as the number of one year citations in a journal divided by the number of articles published in that journal during the last two years.
Dear professor , The impact factor is calculated by dividing the number of citations in the journal citation report per year by the total number of articles published in the past-previous 2 years. A two year time period may over or underestimate the strength of the journal .
Wee Leng Gan
2 years ago
Posttransplantation anemia ( PTA ) is common among kidney transplant recipients.
Early PTA is defined as anemia which develops up to 6 months after transplantation and is the predictor for late PTA
Late PTA is defined as anemia which develops after 6 months and associated with impaired graft function
Iron deficiency being the major contributor for IDA.
PTA is associated with increase mortality, reduced graft survival, and a decline in GFR.
Treatment of PTA should probably begin as soon as possible with ESA and IV Iron. The optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL.
Level 5 evidence.
Impact factor is a scientometric index that reflects the yearly mean number of citations of a journal in the last two years.
Nazik Mahmoud
2 years ago
Post transplant anemia PTA is a common problem,prevalence range from 20-50%
the main cause is iron deficiency
the target Hb should be more than 13g/dl
full panel investigation of serum iron,TIBC,B12 ,folate ,retics count,bilirubin and lactate dehydrogenase
treatment with replacement of the deficit and erythropoietin stimulating agent.
Level 5 evidence
Fatima AlTaher
2 years ago
post transplantation anemia is a common health problem that affect up to 50 % of kidney recipients and defined as HB <12g/dl in females and <13 g/dl in males. Post transplantation anemia has negative impact on graft survival, GFR and recipient mortality specially in severe anemia.
Post transplantation anemia is classified into early (during 1st 6 month after transplantation) and late (after more than 6 months from transplantation). Causes of post transplantation anemia
1- Early onset: mainly due to iron deficiency, poor nutrition, perioperative blood loss and increase erythropoietin production from the graft stimulating erythropoiesis.
2- Late onset anemia:
iron deficiency, myelosuppressive effect of IS drugs, infection, inflammation and decrease graft function Risk factors for post transplantation anemia
1- Early onset anemia is related to female sex, hypochromic RBCs before transplantation and low e GFR.
2- Late onset anemia: early onset anemia is a risk factor for late onset anemia, female patient, donor age, S Cr
Nutritional deficiency including B12 and folic acid Diagnosis of post transplantation anemia
Same approach as non-transplant patients
1- CBC, iron profile, vit B12 and folic acid levels, reticulocytes, comb test, LDH Treatment
No specific KDIGO recommendations for treatment of post transplantation anemia but most studies recommend correct to HB level 13-15 g/dl through replacement of iron, B12 and folic acid in case of their deficiency and consider erythropoietin therapy to reach target HB.
-Level of evidence is V
-Impact factor is used to express the scientific importance of a journal through measuring the frequency of citation of this journal articles during certain time period.
Alyaa Ali
2 years ago
Post transplant anemia PTA
Prevelance 20 to 51%
Early PTA is anemia which develops up to 6 months after transplantation.
Late PTA is anemia which develops after 6 months.
Anemia is defined as hemoglobin levels< 12g/ dl in women and < 13 g/dl in men.
Causes and predictive factors for PTA
Early PTA occurs due to iron deficiency which occurs secondary to depletion of iron stores before transplant, perioerative blood loss and poor nutrition or may be secondary to increased iron utilization with onset of erythropoiesis.
Late PTA due to reduced graft function and development of renal insufficiency, iron deficiency, inflammation, infection , Immunosuppressive drugs ( MMF and Azathioprine) and medications affecting the renin angiotensin aldosterone systems( ACEi , ARBs ) , Trimethoprim sulfamethoxazole and Ganciclovir.
Outcomes of patients with PTA
PTA is associated with reduced mortality, reduced graft survival and decline of GFR.
Anemia was independent risk factor for LVH 1 to 5 years after transplantation. LVH and anemia were associated with a significant risk of death.
Diagnosis
Assessed for usual causes of anemia in non transplant patients
RBC indicies , reticulocyte count , serum iron , transferrin, transferrin saturation, serum ferritin , folate , vitamin B12, haptoglobulin and LDH.
Full anemia work up 3 months post transplant vfor Early detection and early management
Management.
The optimal target hemoglobin level in kidney transplantation is higher the target in haemodialysis and should be up tom12.5 to 13 gm/dl.
With using erythropoiesis – stimulating agents ( ESA ) and iron if indicated.
Impact factor is the average number of citations per year to the recent articles published in that journal.
Last edited 2 years ago by Alyaa Ali
Hinda Hassan
2 years ago
Anemia is defined by WHO as hemoglobin levels < 12 g/dL in women and < 13 g/dL in men. It can occur early (up to 6 months after transplantation) with 50% prevalence and late (after 6 months) with 23–35% prevalence. Causes of and Predictive Factors for post-transplant anemia (PTA)
Early PTA causes are is usually due to iron deficiency due to depletion of iron stores before transplantation, perioperative blood loss, poor nutrition and increased iron utilization with the onset of erythropoiesis.
Late PTA is associated with impaired graft function , iron deficiency, inflammation and infection, immunosuppressive medications, RAS I, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir
factors associated with early PTA included: female sex, lower eGFR , and hypochromic red blood cells.
Factors significantly associated with late PTA included early PTA, graft function; donor age, the use RAS I , the use of immunosuppressive drugs such as mycophenolate mofetil and azathioprine, a recent infection, 3-month creatinine levels and female sex Outcomes of Patients with PTA
Mortality and Graft Failure
Cardiovascular Morbidity, left ventricular hypertrophy and de novo congestive heart failure
GFR Decline Diagnostic Evaluation
1- red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12,
2- tests for presence of hemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin).
3- specific causes of anemia such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc
4- a full anemia work-up approximately 3 months post transplantation for early recognition Treatment of PTA
The management of PTA starts with diagnosis and treatment of all reversible causes .Hb target is 12.5 – 14 g/dL
KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL [40]. The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative and targeting (NKFKDOQI) guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/ dL [45]. Again, no specific recommendation was made for transplant recipients.
The CAPRIT trial in transplanted patients suggest that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL.
level of evidence is 5 Impact factor is used to evaluate the relative journal importance and to measure the frequency of citation of its average article in a particular time period.
Asmaa Khudhur
2 years ago
Posttransplantation Anemia in Kidney Transplant Recipients
Prevalence and Epidemiology:
PTA is widespread, with an incidence ranging from 20-51% depending on the time post-transplant.
Hemoglobin (Hb) levels below 12 g/dL for women and 13 g/dL for males are considered anemic by the World Health Organization (WHO) and the American Society of Transplantation, respectively.
Up until 8 years following transplantation, the frequency of late PTA reduces to about 23-35% at various times.
Causes of and Predictive Factors for PTA:
The typical definition of early PTA is anemia that appears up to six months following transplantation.
It is primarily brought on by a lack of iron.
Anemia that manifests after six months is referred to as late PTA. and it might not show up for up to 8 years.
Late PTA has been linked to diminished graft function and the emergence of renal insufficiency.
Other factors that may contribute to anemia include iron deficiency, infection, immunosuppressive drugs like mycophenolate mofetil, mycofenolic acid, and azathioprione, drugs that affect the renin-angiotensin-aldosterone system like angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobials like trimethoprim-sulfamethoxazole, and antivir
Predictors of PTA:
female sex ,lower eGFR ,hypochromic red blood cells
Early PTA and the use of a living donor as the source of the transplant were both protective factors that were also strongly associated with late PTA (2 years after the transplant).
age of the donor (especially if over 60), use of ACE inhibitors or angiotensin receptor blockers, recent infection, and use of immunosuppressive medications such mycophenolate mofetil and azathioprine.
Etiology of PTA:
The most frequent contributing cause to early PTA is iron insufficiency.
Iron insufficiency can arise for a variety of reasons, including inadequate iron storage at the time of transplantation, blood loss during surgery, increased iron usage with the onset of erythropoiesis, and inadequate diet.
In various investigations, vitamin B12 deficiency was identified as the root cause of PTA in 17–24% of individuals.
10% of the cases in our study were caused by folic acid deficiency, which is a comparatively low percentage compared to the 23-41% described in previous studies.
Acute renal injury, which accounted for 11.4% of instances of PTA, and acute rejection, which accounted for 4% of cases. In 19% of cases, infections were the root cause of anemia.
Outcomes of Patients with PTA:
PTA is linked to decreased GFR, decreased graft survival, and lower death.
The severity of the anemia and its specific causes are linked to the connection with mortality.
Diagnostic Evaluation :
Red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12, as well as tests for the presence of hemolysis (haptoglobin) when clinically indicated, are used to evaluate the usual causes of anemia in non-transplanted patients (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin). Additionally, it is important to look for any specific probable reasons of anemia that may be unique to people who have had a kidney transplant, such as the use of immunosuppressive and antimicrobial medicines, concurrent infections, etc.
Treatment of PTA:
All reversible causes should be diagnosed and treated.
Several issues should be addressed:
Target Hb level for treatment
Type of treatment
anemia (Hb <12.5 g/dL) was significantly associated with mortality in patients with and without ESA. In patients without ESA.
A spontaneous increase in Hb was linked to lower mortality at any level in individuals without ESA. Improvement in anemia (Hb up to 12.5 g/dL) in individuals using ESA was also linked to a lower mortality rate.
As with CKD patients, if ESA is started, the iron status should be determined and the iron stores should be filled.
Whether intravenous iron is superior to orally taken iron in the context of transplantation is a matter of debate.
As soon as possible following a kidney transplant, PTA treatment should start.
The ideal goal Hb level for kidney transplant recipients with anemia should likely be between 12.5 and 13 g/dL, which is higher than the target advised for CKD. It is necessary to have appropriate treatment with ESA and intravenous iron in order to meet this goal.
Level 5
Imapct factor can be calculated by the number of citations received by the article in one year divided by total number of cited articles in the same journal.
Mohammed Sobair
2 years ago
Introductions:
Posttransplant anemia is common problem, associated with increase mortality and graft dysfunction. Prevalence:
Between 21 -50perecdnt.hemoglobin less than 13 in male and 12 mg/dl is define anemia.
Early posttransplant anemia occur before 6 months and late after 6 months . Etiology. And risk factor:
Most common. Due to iron deficiency either pre transplant or due to blood loss during operation or nutritional deficiency .also increased utilization of iron postarnsplant can predispose to iron deficiency.
Vitamins B deficiency and folic acid deficiency. Is less common cause.
Other cause of anemia as infection and drugs should ask be considered. Risk Factors :
Female gender and early posttransplant anemia is known risk factors in addition to glomerular filtration rate.
Complication of PTA:
Increased morality.
Heart failure.
Left ventricular hypertrophy.
Reduce graft function .
Diagnoses:
Baseline hematological indices
Hemoglobin MCV MCHC,iron study ,ferritin, Saturation
In addition to reticulocyte count ,haptoglobin .
Serum vitamin b and folic acid.
Treatment:
Treatment. Of underlying cause.
Iron and ESA to keep hemoglobin level between 12 _13gram.
Level of evidence 5.
Impact factor is total number of citation over last two years divided by number of articles
published in the journal .
Dalia Ali
2 years ago
Introduction
Anemia · Kidney transplant · Posttransplantation anemia Abstract
Posttransplantation anemia (PTA) is common among kidney transplant patients. Early PTA is usually defined as anemia which develops up to 6 months after transplantation, and late PTA is defined as anemia which develops after 6 months. There are multiple causes, with iron deficiency being the major contributor. The occurrence of late PTA has been associated with impaired graft function. Early PTA has been shown to be a predictor of late PTA. PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anemia and to specific causes of anemia. Treatment of PTA should probably begin as soon as possible after kidney transplantation. The optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with erythropoiesis-stimulating agents (ESA) and iron is indicated.
Causes of and Predictive Factors for PTA
Early PTA is usually due to iron deficiency. Iron deficiency may be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition. In addition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia
Late PTA is usually defined as anemia that occurs
more than 6 months after transplantation, and it can appear as late as up to 8 years later . The occurrence of late PTA has been associated with impaired graft function and the development of renal insufficiency .Late PTA is predominantly influenced by a reduced allograft function.
Predictors of PTA
Several studies have aimed to find predictors of PTA. In a retrospective study by our group . 266 patients who underwent kidney transplantation at the Rabin Medical Center in Israel, a single tertiary center, during a 4-year period (2008–2011) were included .
Etiology of PTA Iron deficiency is the most common contributing factor for early PTA. Inadequate iron stores at the time of transplantation, blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition all contribute to the occurrence of iron deficiency
Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies . Folic acid deficiency was the cause of anemia in 10%
of the cases in the study by our group [2], which is a relatively low rate compared to the 23–41% reported in other studies .Other causes of PTA in our cohort included acute kidney injury, accounting for 11.4% of cases, and acute rejection, accounting for 4% of cases. Infections were the cause of anemia in 19% of cases
Outcomes of Patients with PTA Mortality and Graft Failure
PTA has previously been shown to be associated with the composite outcome of all-cause mortality and graft loss. However, while almost all of the studies have shown a significant correlation with graft failure, results regarding the association between anemia and mortality are inconsistent.
Cardiovascular Morbidity
A retrospective Canadian cohort study conducted in 473 renal transplant recipients showed that anemia and was an independent risk factor for left ventricular hypertrophy (according to Cornell electrocardiographic voltage criteria) 1–5 years after transplantation
GFR Decline In the retrospective study by our group, there was a
decline of eGFR with time in patients with anemia. There was a difference of 5.26 mL/min/1.73 m2 in eGFR between 6 months and 2 years. The eGFR in anemic patients declined by 2.26 mL/min/1.73 m2 while the eGFR increased in nonanemic patients
Diagnostic Evaluation
The diagnostic evaluation of renal transplant recipients should include an assessment for “the usual” causes of anemia as with nontransplanted patients, i.e., red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin). In addition, specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc., should be sought. Based on published evidence, a full anemia work-up approximately 3 months post transplantation is indicated as early recognition and treatment may improve the prognosis.
Treatment of PTA
The management of PTA starts with diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause. However, there is no specific recommendation for the treatment of kidney transplant recipients
Several issues regarding specific treatment should be addressed. Most importantly, the target Hb level for treatment, followed by the type of treatment, i.e., erythropoiesis-stimulating agents (ESA) and/or iron, should be determined.
The results of the CAPRIT trial are different from
those observed in larger trials in the CKD population. The Correction of Hemoglobin and Outcomes in Renal Insufficiency (CHOIR) trial included 1,432 CKD stage 3–4 patients who were randomized to achieve a target Hb level of 13.5 or 11.3 g/dL using epoetin-α. The Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT) included 4,038 patients with type 2 diabetes and CKD stage 3–4 to achieve a target Hb. Patients were randomized to either darbepoetin-α to achieve an Hb target of 13.0 g/dL or placebo with rescue darbepoetin-α when the Hb concentration was < 9.0 g/dL
In conclusion, PTA is a common complication of renal transplant recipients. It is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anemia. Treatment of PTA should begin as soon as possible after kidney transplantation. Based on data derived from the CAPRIT . study and the observational study by Heinze et al. [41], it appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
Level 5
Ahmed Omran
2 years ago
Post transplantation anemia in potential kidney transplant recipients
It occurs:
Early period: within 6 months of transplant .
Late: After 6 months of transplant .
Causes :
iron deficiency is the main cause.
Early PTA can predict occurrence of late PTA. In late PTA, the graft function will be impaired. Whether in the early or late period, PTA can lead to reduced mortality, decreased chances of graft survival, and a reduction in GFR. The risk of mortality is linked to the severity of PTA.
Treatment is to be rapid with reaching the target hemoglobin level, up to 12.5-13 g/dL. Treatment includes ESA and iron.
Once ESA has been started, iron status is to be determined and maintained. It is not established whether IV iron or oral iron is better for transplant recipients.
Treatment should be started as soon as possible after transplant. This is essential for better outcome of transplant and to promote chances of graft survival without complications.
-Narrative review – level of evidence 5.
To calculate the impact factor, the number of citations received by the article in one year is divided by total number of cited articles in the same journal.
Nasrin Esfandiar
2 years ago
Summarization of the article:
An important thing is Post transplant anemia (PTA) with currency between 21-55%. Hemoglobin less than 13 in males and less than12 in females is defined as Anemia. Left ventricular failure, poor long term graft outcomes, low eGFR and Congestive cardiac failure are associated with anemia. The article discusses PTA with currency prognosis, etiology and management.
The currency rate is between 21-55% post-transplant patients. Late PTA is anemia happening more than 6 months after the transplant, which can cause dysfunction of graft and is mostly affected by graft dysfunction. Other factors such as immune suppressants, iron deficiency, ACEi,ARBs antibiotics such as sulphathiazole and trimethoprim and antiviral might affect it.
prognosticators of late PTA can be the usage of ACEi, ARBi, living donor, infections, donor age, female sex, and low eGFR. Early PTA is anemia happening less than 6 months after the transplant. It is caused by nutritional factors, increased iron utilization by new onset erythropoiesis after the transplantation, depleted iron stores pre transplant, and peri operative losses. Poor graft outcome and mortality have a correlation with PTA. Treatment of PTA includes: identification of underlying cause and its treatment, erythropoiesis stimulating agents, aiming for Hb >12.5g/dl, and Iron replacement. The level of evidence provided by this article isReview article Level V
The tool to assess the importance of a journal is the impact factor. It is based on the number of citations to the article of this journal, during a specific period of time. Ratio of the number of citations a journal receives in the last 2 years to the number of publications of that journal in the span of the last 2 years would give us the impact factor. Cites/doc (2 years).
We can use the article from a journal as a citation in different presentations, books, and dissertation. For obvious reason, a new journal won’t have impact factor in the first 2 years which can make a bias.
Jamila Elamouri
2 years ago
Posttransplantation Anemia in Kidney Transplant Recipients
Posttransplantation anemia (PTA) is common with a prevalence of 20–51% at various time points after transplantation.
long-term outcomes of PTA:
Increase rates of all-cause mortality, graft failure, congestive heart failure, left ventricular hypertrophy and a decline in the e GFR.
PTA is not defined uniformly either in term of time or in term of the degree of anemia. However, most studies distinguish between early PTA (within 6 months) and late PTA (after 6 months).
Anemia in most studies is defined as hemoglobin (Hb) levels <12 g/dL in women and <13 g/dL in men. Causes of and Predictive Factors for PTA
Iron deficiency may be caused by depletion of iron stores, perioperative blood loss, and poor nutrition.
The onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
B12 and folate deficiency also may contribute.
The occurrence of late PTA has been associated with impaired graft function and the development of renal insufficiency.
Medications like immunosuppression, ACEi, septrin, ganciclovir. Predictors of PTA
Female sex, lower GFR, donor age, creatinine level, the use of ACE inhibitors or angiotensin receptor blockers, the use of immunosuppressive drugs such as mycophenolate mofetil and azathioprine, and a recent infection. Outcomes of Patients with PTA Mortality and graft failure
PTA has previously been shown to be associated with the composite outcome of all-cause mortality and graft loss. However, while almost all of the studies have shown a significant correlation with graft failure, results regarding the association between anemia and mortality are inconsistent. Cardiovascular Morbidity
Anemia is an independent risk factor for left ventricular hypertrophy. LVH and anemia were associated with a significant risk of death. GFR Decline
There was a decline of eGFR with time in patients with anemia.
Normalization of PTA to an Hb level of 13–15 g/dL reduced the rate of decline of eGFR and the estimated creatinine clearance, progression to end-stage renal disease (ESRD), and improved death-censored graft survival. Diagnostic Evaluation
First evaluate the cause of anemia as in non-transplant recipients.
In addition, specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc., should be sought. Early treatment improve the outcome. Treatment of PTA
The management of PTA starts with diagnosis and treatment of all reversible causes. As such, treatment
should be directed at the underlying cause. However, there is no specific recommendation for the treatment of kidney transplant recipients, erythropoietin and iron therapy are important
There is a study shows that Hgb < 12.5 g/dl was significantly associated with mortality in patients with or without ESA.
Another study shows that normalization of PTA with epoetin-B reduces the rate of decline in GFR, progression to ESRD, and improved death-censored graft survival.
the KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is <10.0 g/dL, with a target Hb level of 11.5 g/dL. However, still no specific recommendation to transplant patients.
In regard to iron therapy; iron deficiency, even without anemia, has been shown to be an independent predictor of mortality in renal transplant recipients. I.v. iron administration after transplantation increased Hb levels and reduced the eGFR decline, both of which were more pronounced in lower Hb levels.
If ESA is initiated, the iron status should be determined and iron stores should be repleted, as with CKD
patients. It is unclear in the transplant setting whether i.v. iron is better than orally administered iron. Conclusion:
PTAis a common complication. It is associated with reduced graft survival, decrease in GFR, and mortality. The target hemoglobin in transplant recipient is higher than for CKD patients (12.5 – 13 g/dl). Treatment with iron and ESA should be started as soon as possible.
Level 5
Impact factor is calculated by dividing the number of citations of articles published by the journal in the last two years divided by the total number of articles published during the same period.
Heba Wagdy
2 years ago
Post transplant anemia (PTA) is a common problem occurring at any time post transplant.
It is associated with increased mortality, graft failure, congestive heart failure, left ventricular hypertrophy and impaired graft function. Prevalence and epidemiology:
PTA occurs in 20-51% of kidney transplant recipients, early PTA occurs up to 6 months after transplant and late PTA occurs after 6 months
It is defined as Hgb<12g/dl in women and <13g/dl in men. Causes and predictive values for PTA:
Iron deficiency usually cause early PTA due to depleted iron stores pre transplant, blood loss perioperatively, poor nutrition and increased iron utilization due to increased erythropoietin produced by the graft.
Late PTA is usually due to impaired graft function, other factors include iron deficiency, inflammation, infection, some immunosuppressive agents, ACE-I and ARB, some antimicrobial and antiviral agents as ganciclovir. Predictors of anemia:
Factors associated with early PTA were female, lower eGFR and hypochromic RBCS.
Factors associated with late PTA was early PTA
In a survey, living donor was protective andHgb was strongly associated with graft function.
Early PTA is a predictor of late PTA suggesting that the better prevention and treatment of early PTA can prevent late PTA. Etiology:
Iron deficiency, the most common cause of early and late PTA.
In a retrospective study, nutritional deficiencies were the most cause of late PTA, iron deficiency, vitamin B12 and folic acid deficiency
Other causes were AKI, acute rejection and infections. Outcomes of patients with PTA: Mortality and graft failure:
PTA is significantly correlated with graft failure and mortality in several studies.
Other studies showed conflicting results regarding association between anemia and long-term mortality but anemia was significantly associated with graft loss. Cardiovascular morbidity:
A retrospective study showed that anemia is an independent risk factor for left ventricular hypertrophy and both were associated with significant risk of death. GFR decline:
In the CAPRIT study, normalization of PTA decreased the rate of decline of eGFR, progression to ESKD and improved death censored graft survival. Diagnostic evaluation:
Red blood cell indices, reticulocyte count
Serum iron, TIBC, percent saturation and serum ferritin
Folate and vitamin B12
Tests for presence of hemolysis when clinically indicated
Specific cause of anemia as use of medication or concurrent infection.
It is recommended to perform anemia workup at 3 months post transplant for early recognition and treatment. Treatment of PTA:
No specific recommendations for kidney transplant recipients
Treatment of underlying cause.
KDIGO guidelines recommend initiation of ESA in patients with CKD only when Hgb concentration<10g/dl with target Hgb 11.5
ARCT showed that optimal target Hgb in kidney transplant should be up to 12-13g/dl
Iron deficiency even without anemia was independent predictor of mortality in kidney transplant recipients.
If ESA is initiated, iron status should be determined and stores should be repleted.
A meta analysis showed that IV iron was not associated with increased risk of adverse events or serious infection so can be used in kidney transplant recipients
Level of evidence 5
Ahmed Fouad Omar
2 years ago
Post transplantation anemia (PTA) is common complication that physicians face among post-transplant patient with a prevalence of 20–51%.
It is defined as an Hb of < 12 g/dl for women and < 13 g/dl for men post-transplant.
Long term outcomes of PTA include CHF, LVH, reduced GFR and poor graft and patient survival and increased all-cause mortality .
It can be classified as early ( first 6 months) or late ( after 6months).
Early causes include: low iron stores as a consequence of the CKD and slow increase in the level of newly graft production of erythropoietin , operative blood loss and poor nutritional status.
Late causes include: infections, inflammation, graft dysfunction, iron deficiency anemia and drugs like ACE-I & ARBS, MMF, antibiotics and antivirals.
Predictors include old donor age, living donation, female sex, low eGFR and infections.
Work-up:
– Full history to identify any sources of blood loss, history of infection and drugs
– Full blood count and iron indices(ferritin ,TSAT, Vitamin B12 and folate level).
– Blood film
– Reticulocyte count
– LDH
– Check full occult blood in stool or use Q-FIT test
– Endoscopy if required
Management:
– Aim : hemoglobin -12-13g/dl
– Treatment of the cause
– Vitamin B12 replacement for vitamin B12 deficiency and folate in case of folic acid deficiency.
– Replenish iron stores with I/V iron followed by ESAs
What is the level of evidence provided by this article? The level of evidence: is level V (review article) What is meant by the impact factor of a journal (please in your own words)? The impact factor of a journal means the number of times the articles in a journal are cited over time(total number of cited articles per year divided by the number of publications in two years) time. It shows the relative importance of that journal.
Abdullah Raoof
2 years ago
Posttransplantation Anemia in Kidney Transplant Recipients.
Early PTA is defined as anemia develops up to 6 months after transplantation.
Eate PTA is defined as anemia which develops after 6 months.
There are multiple causes, with iron deficiency being the main cause . The occurrence of late PTA has been associated with impaired graft function.
Early PTA has been shown to be a predictor of late PTA.
PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR.
The optimal target hemoglobin level in kidney
transplant recipients is higher than recommended
in chronic kidney disease and should probably be up to 12.5–13 g/dL.
to achieve this target, appropriate treatment with erythropoiesis-stimulating agents (ESA) and iron is indicated. Introduction:
Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51%.
PTA is negatively associated with
– increased rates of all cause mortality.
– graft failure .
– congestive heart failure .
– left ventricular hypertrophy.
– a decline in the estimated glomerular filtration rate (eGFR). Prevalence and Epidemiology:
Anemia defined as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men.
The prevalence is about 50%. Causes of and Predictive Factors for PTA:
Early PTA is usually due to iron deficiency. Late
PTA is mainly caused by a reduced allograft dysfunction.
other factors that can be acause
– iron deficiency,
– inflammation and infection,
– Medication- immunosuppressive medica tions(mycophenolate mofetil, mycofenolic acid, and azathioprione),
-Anti hypertensives drug (ACEI and ARB) antimicrobial agents such as trimethoprim-sulfamethoxazole and antiviral agents such as ganciclovir . Etiology of PTA:
Iron deficiency is the most common cause of early PTA. In one study the prevalence of anemia was 34%, and iron deficiency anemia was 13%.
Vit- B12 deficiency was the cause of PTA in 17–24% of patients in several studies. Folic acid deficiency was the cause of anemia in 10% of the anemia cases. Other causes may include:
– acute kidney injury 11.4%.
– acute rejection 4%.
– Infections 19%. Outcomes of Patients with PTA:
Regarding the impact of PTA on graft loss and mortality, the result are conflicting.
Some studies shows that PTA increases graft loss and mortality while other report does not. Some study report that there is association of sever ( but not mild ) anemia with graft loss and mortality. Cardiovascular Morbidity:
PTA is independent risk factor for left ventricular hypertrophy. Left ventricular hypertrophy and anemia were associated with a significant risk of death. Anemia was identified as an independent risk factor for de novo congestive heart failure. GFR Decline:
Some studies report that there was a decline of eGFR with time in patients with anemia.
Other studies also suggests that anemia is associated with a decline of GFR and correction of anemia is associated with a reduction in the rate decline. Diagnostic Evaluation:
Red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitaminB12, and tests for presence of hemolysis (haptoglobin) when clinically indicated.
And specific potential causes that is unique to renal transplant recipients, (use of medications (immunosuppressive and antimicrobial), concurrent infections. Treatment of PTA:
treatment of all reversible causes. There is no specific recommendation for the treatment of kidney transplant recipients.
Erythropoiesis-stimulating agents (ESA) and/or iron, can be used. The target of HB 12g/dl is accepted. HG level above this is associated with increase mortality therefore it is not recommended.
Studies suggest that the optimal target Hb level in kidney transplant recipients with anemia is 12–13 g/dL.
If ESA is initiated, the iron status should be deter mined and iron stores should be repleted . It is unclear in the transplant setting whether i.v. iron is better than orally administered iron. But it is reasonable to treat transplanted patients with i.v. iron. Conclusion:
– PTA is a common complication of renal transplant recipients.
– It is associated with reduced mortality,
-reduced graft survival, and a decline in GFR.
– The association with mortality is related to the severity of the anemia.
– Treatment of PTA should begin as soon as possible after kidney transplantation.
– It appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL.
– In order to achieve this target, ap propriate
-treatment with ESA and i.v. iron should be given.
Q2- it is review article- level of evidence is 5.
Q3-
Is the reflection of the yearly mean number of citations of articles published in the last two years in a given journal . As a journal-level metric, it is frequently used as guide for the importance of a journal within its field; journals with higher impact factor values are given the status of being more important.
Manal Malik
2 years ago
Introduction:
Anaemia after transplantation is about 20-51%
Long term effects of anaemia:
· increase rate of all-cause mortality
· graft failure
· congestive heart failure
· left ventricular hypertrophy and decline in the eGFR causes of and predictive factors for PTA:
early PTA is due to iron deficiency may be caused by depletion of iron stores before transplantation.
PTA is usually defined anaemia occurs more than 6 months after transplantation.
Late PTA caused by allograft function other than factors cause anaemia in post transplantation: infection, immunosuppression medication, medication affecting renin-angiotensin-aldosterone system, and antiviral such as ganciclovir.
Iron deficiency anaemia is the most common cause for early PTA.
B12 deficiency reported to be cause of PTA in 17-24% of patients in several studies.
Folic acid was the cause of anaemia in 10% of the cases in study group.
Other causes of PTA:
1. acute kidney injury
2. acute rejection
3. infections Outcomes of patients with PTA:
Several studies showed that there is association with mortality.
A retrospective series 1023 transplant recipients after 3 months was associated with mortality and graft failure. CVS mortality:
A retrospective cohort study is in depend risk factor for left ventricular hypertrophy. GFR decline:
In retrospective study by a group there was a decline of eGFR with time in patients with anaemia. Treatment of PTA:
Nonspecific recommendation of kidney transplant recipient.
CVS reduction early anaemia treatment Epoetin beta.
Kidigo guidelines recommended ESA when Hb<10g/dl
Target Hb in transplant 12-13 g/dl
If ESA started the non-store should repleted. Conclusion:
PTA associated with reduced mortality, reduced graft survival, and a decline in GFR. Target Hb 12-13g/dl. Treatment with ESA and I.V iron.
the leve 5
the impact factor is measured by dividing the number of citations in the journal citation report per year by the total number of articles published in the two previous years.
CARLOS TADEU LEONIDIO
2 years ago
Briefly summarise this article
Post-transplant anemia is a common event and is related to several factors, the most common being depletion of iron stores. Another very common motivation is the use of different classes of drugs that can induce some cytopenia due to myelotoxicity, or even opportunistic infections.
The value of anemia tolerated for post-transplantation is much lower than that tolerated for patients with chronic kidney disease. Anemia in most studies is defined as hemoglobin (Hb) levels < 12 mg/dl in women and < 13 mg/dl in men according to the criteria of the World Health Organization (WHO) and the American Society of Transplantation. And it is divided between early anemia (appearance up to 6 months) or late (appearance after 6 months).
And although studies have not proven an association between anemia and mortality, other outcomes such as graft failure, cardiovascular morbidity and decline in Glomerular Filtration Rate have proven association.
The diagnostic evaluation of renal transplant recipients should include an assessment for “the usual” causes of anemia as with nontransplanted patients, i.e., red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin). In addition, specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc. And the management of anemia starts with diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause. However, there is no specific recommendation for the treatment of kidney transplant recipientes.
· What is the level of evidence provided by this article?
Level 05 – narrative review
What is meant by the impact factor of a journal (please in your own words)?
Impact factor is an attempt to measure the impact that a publication has by counting the times that its articles have been cited, establishing a rank with those that presented the highest number of citations.
Hamdy Hegazy
2 years ago
Briefly summarise this article
Incidence of post-TX anaemia: 20-50% and is associated with increased all cause mortality, graft failure, CHF, LVH. Causes of early(within 6 months) post TX anaemia: peri-operative blood loss, iron deficiency, increased iron consumption because of increased EPO from new renal graft. Cause of late (more than 6 months) post TX anaemia: infection, inflammation, iron deficiency, medications (MMF, MFA, AZA, ACE.I, ARBs, TMP/SMX, ganciclovir). Anaemia work up: FBC, RBC Indices, Reticulocytic count, Iron profile, Folate, B12, Haptoglobin, LDH, bilirubin.
Treatment of the cause
What is the level of evidence provided by this article?
Level II, retrospective cohort study.
Ahmed Abd El Razek
2 years ago
Introduction
The prevalence of post transplantation anaemia is about 20–51%. Post transplantation anaemia PTA is associated with worse long-term outcomes: increased rates of all-cause mortality, graft failure, congestive heart failure, left ventricular hypertrophy, as well as decline in the estimated glomerular filtration rate (eGFR).
Prevalence and Epidemiology
Early PTA is apparent up to 6 months after transplantation while late PTA occurs after 6 months. The prevalence of early PTA is about 50%, on the other hand late PTA declines to about 23–35% at various time points up until 8 years after transplantation.
Causes of and Predictive Factors for PTA
Early PTA is mostly due to iron deficiency which is enhanced by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition along with the improvement of iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin.
The occurrence of late PTA is correlated to impaired graft function and the development of renal insufficiency. Other factors may coexist potentiating PTA as iron deficiency, inflammation, infection, immunosuppressive agents, trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir.
Predictors of PTA
Female sex, lower eGFR and hypochromic red blood corpuscles are surrogates for PTA while kidneys derived from living donations acted as a protective shield against PTA.
Early PTA is also a predictor of late PTA, so the better the prevention and treatment of early PTA the less exposure to late PTA.
Etiology of PTA
Iron deficiency is the most common contributor to late PTA according to many studies. Vitamin B12 and folic acid deficiency were reported as other less contributing causes of PTA besides infections and immunosuppressive medications.
Outcomes of Patients with PTA
Mortality and Graft Failure
Anemia was significantly associated with mortality, graft failure of average follow-up of 6 years in addition to the increased risk of death.
Cardiovascular Morbidity
Anemia and left ventricular hypertrophy as an independent risk factor for cardiovascular morbidity were studied at 1–5 years after transplantation that was associated with a significant risk of death. Anemia also was identified as an independent risk factor for de novo congestive heart failure for previously known cardiac free patients.
GFR Decline
The estimated difference of in eGFR between 6 months and 2 years in anemic patients declined by 2.26 mL/min/1.73 m2 while the eGFR improved in nonanemic patients.
Normalization of PTA to an Hb level of 13–15 g/dL reduced the rate of eGFR decline, the estimated creatinine clearance, progression to end-stage renal disease (ESRD), and improved death-censored graft survival after administration of epoetin-β.
Diagnostic Evaluation
A full anemia work-up 3 months post transplantation is indicated for early recognition and treatment aiming to improve the prognosis. Thus, treatment of PTA should begin as soon as possible after kidney transplantation. To achieve this target, proper treatment with ESA and i.v. iron should be administered.
Level of evidence is 5.
The impact factor of a journal is commonly used to evaluate the suggested relative importance of a journal within its field as well as to assess the frequency which the “average article” in a journal has been cited in a particular time period. The more the journal publishes review articles, the higher the impact factor it will achieve.
Abhijit Patil
2 years ago
Summary:
Post transplantation anemia (PTA)
Early PTA is usually defined as anemia which develops up to 6 months after transplantation
Late PTA is defined as anemia which develops after 6 months.
There are multiple causes, with iron deficiency being the major contributor.
The occurrence of late PTA has been associated with impaired graft function.
Early PTA has been shown to be a predictor of late PTA.
PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR.
The association with mortality is related to the severity of the anemia and to specific causes of anemia.
Treatment of PTA should probably begin as soon as possible after kidney transplantation.
The optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL.
In order to achieve this target, appropriate treatment with erythropoiesis- stimulating agents (ESA) and iron is indicated.
Level of evidence: Level 5
Wadia Elhardallo
2 years ago
Anemia in most studies is defined as hemoglobin (Hb) levels <12 g/dL in women and <13 g/dL in men, in accordance with World Health Organization (WHO) criteria and the American Society of Transplantation
PTA is not defined uniformly either in terms of timing after transplantation or in terms of the degree of anemia. However, most authors suggest distinguishing between early PTA (up to 6 months after transplantation) and late PTA (after 6 months). The prevalence of early PTA is about 50% according to various studies and the prevalence of late PTA declines to about 23–35% at various time points up until 8 years after transplantation.
Early PTA is usually due to iron deficiency. Iron deficiency may be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition In addition, increased iron utilization with the onset of erythropoiesis. Late PTA is predominantly influenced by a reduced allograft function. However, other factors, i.e., iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia .
Outcomes of Patients with PTA:
Mortality and Graft Failure : PTA has previously been shown to be associated with
the composite outcome of all-cause mortality and graft
loss. However, while almost all of the studies have shown
a significant correlation with graft failure, results regarding the association between anemia and mortality are inconsistent. Several studies have documented an association with
mortality. A retrospective multicenter analysis using a French database that included 4,217 transplant recipients showed that PTA at 12 months was associated with mortality and graft failure . A prospective cohort study of 938 kidney transplant recipients in Hungary showed PTA
to be associated with mortality and graft failure at the 4-year follow-up .in a large
retrospective analysis of 2,031 transplant recipients in Austria, anemia was significantly associated with mortality and graft failure at a median follow-up of 6 years
Cardiovascular Morbidity: A retrospective Canadian cohort study conducted in 473 renal transplant recipients showed that anemia andwas an independent risk factor for left ventricular hypertrophy (according to Cornell electrocardiographic voltage criteria) 1–5 years after transplantation. Left ventricular hypertrophy and anemia were associated with a significant risk of death. Another retrospective cohort study conducted in 2 Canadian centers included 638 consecutive adult renal transplant recipients who were free of cardiac disease 1 year after transplantation. Anemia was identified as an independent risk factor for de novo congestive heart failure
GFR Decline: In the retrospective study by our group, there was a
decline of eGFR with time in patients with anemia. There was a difference of 5.26 mL/min/1.73 m2 in eGFR between 6 months and 2 years. The eGFR in anemic patients
declined by 2.26 mL/min/1.73 m2 while the eGFR increased in nonanemic patients [1]. In the prospective randomized CAPRIT (Correction of Anemia and Progression of Renal Insufficiency in Transplant Patients) trial , patients were randomized to receiving epoetin-β with a target of 13–15 or 10.5–11.5 g/dL. Normalization of PTA to an Hb level of 13–15 g/dL reduced the rate of decline of eGFR and the estimated creatinine clearance,
progression to end-stage renal disease (ESRD), and improved death-censored graft survival. This suggests that anemia is associated with a decline of GFR and correction
of anemia is associated with a reduction in the rate decline.
What is the level of evidence provided by this article?
Level 5 * review
What is meant by the impact factor of a journal (please in your own words)?
Impact factor is used to evaluate relative importance of the journal in the field
Reem Younis
2 years ago
Briefly summarise this article
-Posttransplantation anemia (PTA) prevalence is 20–51% at various time points after transplantation .
-PTA has been shown to be negatively associated with the following long-term outcomes: increased rates of all-cause mortality , graft failure , congestive
heart failure , left ventricular hypertrophy , and a decline in the estimated glomerular filtration rate (eGFR) .
-Early PTA (up to 6 months after transplantation) and late PTA (after 6 months) .
-Early PTA is usually due to iron deficiency (Inadequate iron stores at the time of
transplantation, blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition all contribute to the occurrence of iron deficiency).
-The occurrence of late PTA has been associated with impaired graft function
and the development of renal insufficiency .
-Late PTA is predominantly due to a reduced allograft Function , iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin- aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir.
-Factors associated with early PTA included: female sex , lower eGFR , and hypochromic red blood cells.
– Factors significantly associated with late PTA (2 years after transplantation) included early PTA, and a living donor as the transplantation source was protective .
-Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies and folic acid deficiency was the cause of anemia in 10% of the cases.
– PTA at 12 months was associated with mortality and graft failure .
– Both severe and mild anemia were associated with graft failure.
-Left ven tricular hypertrophy and anemia were associated with a significant risk of death and anemia was an independent risk factor for de novo congestive heart failure .
– Anemia is associated with a decline of GFR and correction of anemia is associated with a reduction in the rate decline.
-The diagnostic evaluation of renal transplant recipients should include an assessment for red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when
clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin).
-The management of PTA starts with diagnosis and treatment of all reversible causes. However, there is no specific recommendation for the treatment of
kidney transplant recipient.
-Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD and improved death-censored graft survival.
-Both the CHOIR trial and the TREAT demonstrated an increased risk of
cardiovascular events and no delay in progressive renal failure by targeting normalization of Hb with ESA therapy.
-Based on these studies the KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL .
-The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative and targeting (NKFKDOQI) guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/ dL .
-No specific recommendation was made for transplant recipients.
-The CAPRIT trial in transplanted patients suggest that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL.
-Iron deficiency, even without anemia, has been shown to be an independent
predictor of mortality in renal transplant recipients .
-It is retrospective cohort study that included 81 patients who received intravenous (i.v.) iron after transplantation between 2000–2009; i.v. iron
administration after transplantation increased Hb levels and reduced the eGFR decline, both of which were more pronounced in lower Hb levels. What is the level of evidence provided by this article?
Level 5 What is meant by the impact factor of a journal (please in your own words)?
In any given year, the two-year journal impact factor is the ratio between the number of citations received in that year for publications in that journal that were published in the two preceding years and the total number of “citable items” published in that journal during the two preceding years.
Nandita Sugumar
2 years ago
Summary – Posttransplantation anemia in kidney transplant recipients
This article revolves around post transplant anemia developing in kidney transplant recipients. This can be found in different time frames following the transplant.
Early period, i.e., within 6 months of transplant – early PTA
After 6 months of transplant – late PTA
Causes :
iron deficiency – major reason
Early PTA can predict development of late PTA. If late PTA occurs, it is possible that graft function will be impaired. Whether in the early or late period, any kind of PTA can lead to reduced mortality, decreased chances of graft survival, and a reduction in GFR. The risk of mortality in each of these patients is linked to the severity of PTA.
Treatment is to be prompt with restoration of target hemoglobin level, up to 12.5-13 g/dL. Treatment options include ESA or erythropoietin stimulating agents and iron.
Once ESA has been started, iron status is to be determined and repleted. It is not confirmed whether IV iron or oral iron is better for transplant recipients.
Treatment should be started soon after transplant without delay. This is essential for good outcome of transplant and to boost chances of graft survival without unnecessary complications.
Level of evidence
Narrative review – level of evidence 5.
Impact Factor
Impact factor is the average number of times a given article has been cited within the JCR year. To calculate the impact factor of an article, the number of citations received by the article in one year is divided by total number of cited articles in that journal.
Naglaa Abdalla
2 years ago
Post-transplant anemia (PTA) is common clinical problem among kidney-transplant patients with prevalence 20 – 51 % at various time points.
According to WHO criteria and the American Society of Transplantation, anemia is defined as hemoglobin (Hb) levels below < 12 g/dl in women and < 13 g/dl in men. Classification :
1- Early PTA : occur up to 6 months after transplantation
2- Late PTA : occur after 6 month Causes of PTA:
Early PTA can be caused by :
1- iron deficiency
2- operation associated bleeding
3- poor nutrition
4- low erythropoietin secretion of the new graft.
Late PTA causes include:
1- Impaired graft function and renal failure
2- Iron deficiency, vitamin B12 and folic acid deficiencies.
3- Infection and inflammation
4- Immunosuppressive drugs like (mycophenolate mofetil, mycofenolic acid, and azathioprione),
5- Medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting
enzyme inhibitors and angiotensin receptor blocker
6- Antimicrobial agents such as trimethoprim-sulfamethoxazole,
7- Antiviral agents such as ganciclovir. Complications of PTA:
1- Increased mortality and graft loss
2- Cardiovascular morbidity
3- Decline of GFR Diagnosis of PTA:
1- CBC and red blood indices
2- Reticulocyte count
3- serum iron, total iron-binding capacity (transferrin), transferrin saturation, serum ferritin
4- Folate level and vitamin B12
5- Hemolysis indicators like haptoglobin, elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin. Treatment of PTA :
Should be directed according to the underlying cause.
There is no specific recommendation for the treatment unlike the situation in chronic kidney disease.
What is meant by the impact factor of a journal ?
done for journal evaluation within its field after completing the minimum of 3 years of publication, that the journal which publishes more review articles will get highest impact factors and thus will be more important than than those with lower ones. .
It is calculated by dividing the number of citations in the JCR year by total number of articles published in the previous years.
IF = Number of citations in y /Sum of publications in last 2 year
MICHAEL Farag
2 years ago
Anemia in most studies is defined as hemoglobin (Hb) levels <12 g/dL in women and <13 g/dL in men, in accordance with World Health Organization (WHO) criteria and the American Society of Transplantation. Post-transplant anemia can be divided into Early PTA (up to 6 months after transplantation) and late PTA (after 6 months) Causes of and Predictive Factors for PTA
Early PTA is usually due to iron deficiency which can be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition. In addition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
Late PTA is usually defined as anemia that occurs more than 6 months after transplantation, and it can appear as late as up to 8 years later. The occurrence of late PTA has been associated with impaired graft function and the development of renal insufficiency.
However, other factors, i.e., iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia
Treatment of PTA The management of PTA starts with diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause. However, there is no specific recommendation for the treatment of kidney transplant recipients
What is meant by the impact factor of a journal (please in your own words)?
The impact factor (IF) is a measure of the frequency with which the average article in a journal has been cited in a particular year
The impact of a journal in a particular year =
The total number of its articles were cited within previous 2 years
—————————————————————————————- ÷
The total number of citable articles in the journal during same those 2 years
What is the level of evidence provided by this article? Level V
Huda Al-Taee
2 years ago
Briefly summarise this article
Posttransplantation anaemia( PTA) is common among kidney-transplant patients, with a prevalence of 20–51%.
It is negatively associated with the following long-term outcomes: increased all-cause mortality rates, graft failure, congestive heart failure, left ventricular hypertrophy, and a decline in the eGFR.
Prevalence and Epidemiology
up to 20–51% of patients remain anemic after transplantation at various times post-transplant.
most authors suggest distinguishing between early PTA (up to 6 months after transplantation) and late PTA (after 6 months).
The prevalence of early PTA is about 50% according to various studies and the prevalence of late PTA declines to about 23–35% at various time points up until 8 years after transplantation.
Causes of and Predictive Factors for PTA :
Early PTA is due to iron deficiency anaemia.
Late PTA is due to reduced allograft function, iron deficiency, infection, inflammation, IS medications, other non IS medications such as ACEi, ARB.
Predictors of PTA:
In multivariate analysis, factors associated with early PTA:
female sex
lower eGFR
hypochromic red blood cells
factors associated with late PTA:
early PTA.
a living donor as the transplantation source was protective
Etiology of PTA:
Iron deficiency is the most common cause.
Vitamin B12 deficiency
Folic acid deficiency
ther causes such as acute kidney injury, acute rejection, and infections.
Outcomes of Patients with PTA:
Mortality and Graft Failure:
Almost all of the studies have shown a significant correlation with graft failure, and results regarding the association between anaemia and mortality are inconsistent.
Cardiovascular Morbidity:
anaemia showed to be an independent risk factor for left ventricular hypertrophy in a retrospective study. Also, it was identified as an independent risk factor for de novo congestive heart failure in another study.
GFR Decline:
In a retrospective study, The eGFR in anemic patients declined by 2.26 mL/min/1.73 m2 while the eGFR increased in nonanemic patients.
Diagnostic Evaluation:
red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity, percent transferrin saturation, serum ferritin, folate, and vitamin B12, and tests for the presence of hemolysis (haptoglobin) when clinically indicated.
specific causes for anaemia in post-transplant patients such as medications and infections.
Treatment of PTA:
no specific recommendation for the treatment of kidney transplant recipients.
the target Hb level for treatment, type of treatment, i.e., erythropoiesis-stimulating agents (ESA) and/or iron, should be determine.
treatment should be directed at the underlying cause.
Based on data derived from the CAPRIT study and the observational study, it appears that the optimal target Hb level in kidney transplant recipients with anaemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL.
In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
What is the level of evidence provided by this article?
Level 5 (review article)
What is meant by the impact factor of a journal (please in your own words)
Impact factor is commonly used to evaluate the relative importance of a journal within its field and to measure the frequency with which the “average article” in a journal has been cited in a particular time period.
Hussam Juda
2 years ago
Briefly summarise this article
Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation
PTA associated with
· increased rates of all cause mortality
· graft failure
· congestive heart failure
· left ventricular hypertrophy
· decline in eGFR
There are early PTA (up to 6 months after transplantation) and late PTA (after 6 months)
Definition of anemia: hemoglobin (Hb) levels <12 g/dL in women and <13 g/dL in men
Early PTA is occurring in 50% while late PTA declines to about 23–35% at various time points up until 8 years after transplantation
Causes of and Predictive Factors for PTA
Early PTA is usually due to iron deficiency which could be due to:
· depletion of iron stores before transplantation
· perioperative blood loss
· poor nutrition
· increased iron utilization with the onset of erythropoiesis with slowly increasing
levels of the newly graft-produced erythropoietin
late PTA has been associated with
· impaired graft function and the development of renal insufficiency
· iron deficiency
· inflammation and infection
· immunosuppressive drugs (MMF, MFA, and azathioprione)
· angiotensin-converting enzyme inhibitors and angiotensin receptor blockers
· antimicrobial agents such as trimethoprim-sulfamethoxazole
· antiviral agents such as ganciclovir
Predictors of PTA Risk factors for early PTA: female sex, lower eGFR, and hypochromic red blood cells Risk factors for late PTA: early PTA, Graft dysfunction, Donor age (mainly > 60 y), and female gender
Etiology of PTA
· Iron deficiency is the most common contributing factor for early PTA mostly due to: Inadequate iron stores at the time of transplantation, blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition
· Vitamin B12 deficiency is the cause of PTA in 17–24% of patients
· Folic acid deficiency was the cause of anemia in 10% of the cases
· acute kidney injury in 11.4% of cases
· acute rejection in 4% of cases
· Infections were the cause of anemia in 19% of cases
Outcomes of Patients with PTA
· Severe anemia (Hb <11 g/dL)was associated with mortality while mild anemia was not
· Both severe and mild anemia were associated with graft failure
· anemia an independent risk factor for left ventricular hypertrophy 1–5 years after transplantation
· Left ventricular hypertrophy and anemia were associated with a significant risk of death
· there was a decline of eGFR with time in patients with anemia
Diagnostic Evaluation
red blood cell indices, reticulocyte counts, serum iron, TIBC (transferrin), serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin.
Drug or infection history
Treatment of PTA
· diagnosis and treatment of all reversible causes
· erythropoiesis-stimulating agents (ESA) and/or iron as CKD guidelines
· If ESA is initiated, the iron status should be determined and iron stores should be
repleted, as with CKD patients
· optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL
What is the level of evidence provided by this article?
Cohort study. Evidence level 2
What is meant by the impact factor of a journal (please in your own words)?
It is a calculation indicates the importance of a Journal to its field. IF cannot be calculated for new journals, only after completing of 3 years of publication.
The IF of any journal may be calculated by the formula (e.g., in 2012)
2012 impact factor =A/B
Where A is the number of times articles published in 2010 and 2011 were cited by indexed journals during 2012. B is the total number of citable items like articles and reviews published by that journal in 2010 and 2011 What is the bias involved in relying on the impact factor to assess journals?
IF evaluation is based on a sample that may represent half the whole-of-life citations to some journals, but a small fraction (<10%) of the citations accruing to other journals. This disproportionate sampling means that the IF provides a misleading indication of the true impact of journals, biased in favour of journals that have a rapid rather than a prolonged impact.
abosaeed mohamed
2 years ago
Post-transplantation Anemia in Kidney Transplant Recipients(PTA)
– Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% – can be divided into: · Early PTA: developed within 6 months post-transplant . · Late PTA: developed after 6 months post-transplant . – The optimal target Hb level in KTR >>12.5 to 13 g/dl.
Causes :
– Iron deficiency as a result of depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition, increased iron utilization. – chronic allograft injury , iron deficiency, inflammation, infection, immunosuppressive medications, antiviral agents (ganciclovir), TMP/SMX, ACEI and ARBs.
Predictors :
– Early PTA: female sex and low GFR. – Late PTA: early PTA , female sex , 3-months creatinine level (SCr >2mg/dl), donor age >60, infection and drugs ( use of MMF, AZA, ACEI, TMP/SMX).
Outcome :
– all cause Mortality and graft failure increased with Hb <11g/dl. – Cardiovascular morbidity( anaemia is an independent risk factor for LVH). – Decline of GFR (The eGFR in anemic patients declined by 2.26 mL/min/1.73 m2 while the eGFR increased in nonanemic patient).
Diagnostic evaluation:
– usual work up : RBCs indices, retics count, iron study, folate and vit B12 level.
– search for Haemolysis: haptoglobin level, retics count, bilirubin and LDH. – Potential causes of anaemia should be sought( drugs, infection).
Management :
– Diagnosis and treatment of all reversible causes. – target>> hb.>>12-13.5 – Iron oral or IV & – erythropoietin stimulating agents
>>>>>Level of evidence >>level 5. The Impact factor (IF) is an index that reflects the yearly mean number of citations of articles published in the last two years in a given journal
Calculation:
– In any given year, the two-year journal impact factor is the ratio between the number of citations received in that year for publications in that journal that were published in the two preceding years and the total number of “citable items” published in that journal during the two preceding years – For example : IF (2020) = citations in 2020 / (publications in 2019 + publications in 2018 )
Theepa Nesam
2 years ago
Posttransplantation anemia (PTA) is common among KTRs, with a prevalence of 20–51%
It has been shown to be negatively associated with: 1. Increased rates of all cause mortality 2. Graft failure 3. Congestive heart failure 4. LVH 5. Decline in eGFR Prevalence and Epidemiology KT may correct anaemia, but up to 20–51% of patients remain anaemic after transplantation
Two main types: 1. Early PTA (up to 6 months after transplantation)- 50% of cases 2. Late PTA (after 6 months) occurs in 23-35% Causes of and Predictive Factors for PTA 1-Early PTA is usually due to IDA 2-Late PTA -associated with impaired graft function and the development of renal insufficiency. Late PTA is predominantly influenced by a reduced allograft function. other factors: iron deficiency inflammation and infection IS- Mycophenolate mofetil, mycofenolic acid, and azathioprione medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers antimicrobial – as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anaemia Predictors of PTA · Female sex. · Lower eGFR. · Hypochromic red blood cells Factors significantly associated with late PTA (2 years after transplantation) included: · Early PTA, (HR 0.601; 95% CI 0.453–0.799, for every · Living donor as the transplantation source wasprotective
· Donor age above 60 years
· Use of ACE inhibitors or angiotensin receptor blockers
· Use of IS – mycophenolate mofetil and azathioprine.
· Recent infection
Aetiology of PTA · IDA – common contributing factor for early PTA. Due to: 1. Inadequate iron stores at the time of transplantation. 2. Blood loss during surgery. 3. Increased iron utilization with the onset of erythropoiesis. 4. Poor nutrition · Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies. · Folic acid deficiency was the cause of anaemia in 23-41% · Acute kidney injury, accounting for 11.4% of cases, and · Acute rejection, accounting for 4% of cases. · Infections were the cause of anaemia in 19% of cases. Outcomes of Patients with PTA Mortality and Graft Failure associated with the composite outcome of all-cause mortality and graft loss. However, while almost all the studies have shown a significant correlation with graft failure, results regarding the association between anaemia and mortality are still unclear Cardiovascular Morbidity Anaemia – independent risk factor for de novo congestive heart failure and left ventricular hypertrophy eGFR Decline associated with a decline of GFR and correction of anaemia is associated with a reduction in the rate decline Diagnostic Evaluation The classic causes of anaemia as with non transplanted patients Red blood cell indices, Reticulocyte counts Serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin. Folate Vitamin B12 Tests for presence of haemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin). 2. Specific potential causes of anaemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infection Treatment of PTA Treatment should be directed at the underlying cause\ Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD and improved death-censored graft survival. Compared to the partial-correction group, the complete-correction group had a smaller decrease in the estimated creatinine clearance (i.e., 5.9 vs. 2.4 mL/ min/1.73 m2), a lower rate of ESRD (i.e., 21 vs. 4.8%), and a higher death-censored graft survival (i.e., 80 vs. 95%). There was also a significant improvement in quality of life in the full-correction group. Regarding cardiovascular outcomes, although the numbers were small, there were no cardiac disorders (cardiac failure, arrhythmia, or myocardial infarction) in the full-correction group compared to 4 patients (8%) in the partial-correction group, In conclusion, PTA is a common complication of KTRs. It is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anaemia. Treatment of PTA should begin as soon as possible after kidney transplantation. Based on data derived from the CAPRIT study and the observational study by Heinze et al, it appears that the optimal target Hb level in kidney transplant recipients with anaemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. To achieve this target, appropriate treatment with ESA and i.v. iron should be given.
What is the level of evidence provided by this article?
level 4.
Eusha Ansary
2 years ago
Early PTA is usually defined as anemia which develops up to 6 months after transplantation, and late PTA is defined as anemia which develops after 6 months.
In case of early PTA iron deficiency being the major contributor. The occurrence of late PTA has been associated with impaired graft function. Early PTA has been shown to be a predictor of late PTA. PTA is associated with mortality, reduced graft survival, and a decline in GFR.
Post transplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation and negatively associated with the following long-term outcomes: increased rates of al lcause mortality, graft failure, congestive heart failure, left ventricular hypertrophy, and a decline in the estimated glomerular filtration rate
In early PTA Iron deficiency may be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition. In addition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
The occurrence of late PTA may be caused by iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir. There is observation that early PTA is a predictor of late PTA as well.
Treatment of PTAshould be directed at the underlying cause.
Level 5 evidence
Impact factor can evaluate the importance of a journal. It is calculated by dividing the number of citation in the previous two years by the number of articles published during this time of a journal.
Yashu Saini
2 years ago
Briefly summarise this article
This article reviews about anemia in kidney transplant recipients after kidney transplantation. The article discusses lot of studies regarding PTA and quotes their observations.
Post transplantation anemia (PTA) is quite common entity and has prevalance to the tune of 20-51% and has deletarious long term outcomes.
PTA has been divided in two categories by some authors.
early PTA – upto 6 months after transplantation
Late PTA – after 6 months of transplantation
Causes of PTA
Early PTA – Iron deficiency anemia
Late PTA – Reduced allograft function, Iron deficiency, Immunosuppresive medications, ACEI, antiviral agents like Gancyclovir
Predictors of PTA
early PTA – Female sex, low eGFR, hypochromic RBC
Late PTA – Early PTA, elevated serum creatinine, elderly age, Immunosuppresive medications, ACEI
Common deficiencies associated with PTA are, iron deficiency, Vit B12 and folic acid deficiency
Outcomes of PTA
Increased mortality and graft failure
Cardiovascular morbidity – LVH,
GFR decline
Diagnostic evaluation: Full anemia workup including RBC indices, reticulocyte count, serum iron, TIBC, transferrin saturation, folate levels, etc.
NOTE: Overall this is not a nicely written article. It just keeps quoting articles but doesnt give any consensus statement at the end. There is no summary table of all included articles. There is also error in language
“The Correction of Hemoglobin and Outcomes in Renal Insufficiency (CHOIR) trial [42] included 1,432 CKD stage 3–4 patients who were randomized to achieve a target Hb level of 13.5 or 11.3 g/dL using epoetin-α.”
I didnt understand this statement.
What is the level of evidence provided by this article?
Its level 6 evidence as its a narrative review in descriptive format.
What is meant by the impact factor of a journal (please in your own words)?
Impact factor is a sort of method of ranking a journal. It depends on the number of times the articles published in a journal have been cited.
In particular, its the average frequency with which article citation has been done in particular year .
Its calculated as follows:
Number of citations of article (published in last 2 years) in journal citation reports divided by total number of articles published in last 2 years.
Rahul Yadav rahulyadavdr@gmail.com
2 years ago
Briefly summarize this article
Prevalence of Post-Transplant Anemia (PTA) varies from 20-51%.
Optimal target Hemoglobin after kidney transplant is above 12g/dL in females and 13g/dL in males (WHO, AST criteria).
PTA is divided into two types depending on its occurrence following varying periods after transplant
Early PTA: Anemia within 6 months post-transplant
· Prevalence 50%
· Causes: Iron deficiency anemia (Depletion of iron stores, Peri-operative blood loss, poor nutrition, increase iron utilization with onset of erythropoiesis post transplant)
· Early PTA is a predictor for late PTA
Late PTA: Anemia 6 months post-transplant
· Prevalence:23-35%
· Causes: Nutritional Deficiencies most common cause (Iron deficiency>Vit B12 def>Folate Def), Infections, certain immunosuppressive drugs(MMF, Mycophenolic acid, azathioprine), ACEI, ARB, certain antimicrobials(TMP-SMX) and antivirals like ganciclovir
· Late PTA has been associated with impaired graft function and reduced graft survival
Outcome of Patients with PTA
· Mortality: related to severity of anemia. Severe(<11g/dL) associated with all-cause mortality while mild doesn’t.
· Graft Failure: Anemia is associate with graft failure (Mild as well as severe)
· Cardiovascular morbidity: associated with LVH, de Novo CHF with significant risk of death
· GFR decline: Anemia associated with GFR decline, estimated creatinine clearance and progression to ESRD and correction reverses it
Diagnosis: Following test as same in non-transplant individuals
1. Complete Blood count
2. Reticulocyte count
3. S.Iron
4. S.Ferritin
5. TIBC(Transferrin)
6. Percent Transferrin Saturation
7. S.Folate
8. S.Vit B12
9. Tests for presence of Hemolysis as indicated (Reduced Haptoglobin, Elevated Reticulocyte count, LDH and indirect Bilirubin)
10. Specific Tests for concurrent infection if clinically indicated
Treatment:
· Treat the underlying causes
· Optimal Target level is 12 to 13g/dL
· No specific recommendation present in literature
· Treat it with ESA and oral/IV iron appropriately. IV iron preferred.
· Iron stores to replete before starting ESA
What is the level of evidence provided by this article?
It is Narrative review article and hence level of evidence in 5
What is meant by the impact factor of a journal (please in your own words)?
The impact factor is a measure of frequency with which the average article in a journal has been cited in a particular year.
Calculation is based on a two-year period and involves number of times articles were cited divided by the number of citable articles.
Calculation of 2021 IF of journal:
A=the number of times articles [published in 2019 and 2020 were cited by indexed journals during 2021
B=Total number of citable articles published in 2019 and 2020
A/B=2021 IF of journal
It is used to evaluate the importance or rank of a journal by calculating the times its articles are cited.
marius Badal
2 years ago
The article was a great one and it deals with post-transplantation anemia (PTA). PTA is common in kidney transplant patients with a prevalence of 20-51%. Early PTA is defined as anemia that develops up to 6 months after transplant while late PTA is defined as anemia that develops after 6 months. The optimal target of hemoglobin level in kidney transplant recipients should be about 12.5-13 g/dl.
There are many causes of PTA and depend on if it is early or late. 1) Early PTA
a) Iron deficiency
b) Inadequate iron stores before transplant
c) Blood loss during the procedure
d) Poor diet or nutrition
e) Increase use of EPO
f) Vitamin B 12 deficiency
g) Folic acid deficiency
h) Infections
i) AKI
j) Acute rejection 2) Late PTA
a) Inflammation
b) Infections
c) Iron deficiency
d) Immunosuppressive medications 3) Other causes
a) Due to medications like ACEI, antiviral medications like ganciclovir
b) Nutritional factors
There are predictors of PTA because of females, lower GFR, and hypochromic RBC. It was noted that elevated serum creatinine levels greater than 2mg/dl may be a cause of PTA and is frequent in donors aged above 60 years, medications like ACEI, immunosuppressives like MMF and AZA and infections or sepsis
The outcome of post-transplant patients depends on mortality and graft failure, cardiovascular morbidity, and a decrease in GFR.
HOW DO WE DIAGNOSE A PATIENT WITH PTA
The protocol of anemia is almost like that in patients that are non transplanted. One must study or do the required studies:
1) Haemoglobin levels that are RBC indices and reticulocyte counts
2) Serum iron, TIBC, ferritin, transferrin saturations, etc.
3) Vitamin B12 and folate level
4) Coomb tests
5) Test for hemolysis
6) LDH levels
7) Medications levels like immunosuppressive medications
Treatment of PTA/:
It involves treatment of the cause.
Provide proper nutrition with vitamin B12, folic acid, etc.
Provide EPO or ESA
The article was a level 5
The impact factor of a journal is commonly used to evaluate the relative importance of a journal within its field and to measure the frequency with which the average article in a journal has been cited in a particular period. The higher the IF the better it is for the article.
amiri elaf
2 years ago
# Briefly summarise this article
*This review provided updated information regarding the prevalence of post transplantation anemia (PTA) in KT recipients and the causative and predictive factors.
*Early PTA (up to 6 months after transplantation), with prevalence of about 50%.
*Late PTA (after 6 months, and it can appear later up to 8 years later), with prevalence about 23–35%
*The World Health Organization (WHO) criteria and the American Society of Transplantation defined anemia as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men.
*Causes of early PTA is usually due to iron deficiency, due to depletion of iron stores before
Transplantation.
*Perioperative blood loss, and poor nutrition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
*Late PTA is usually associated with impaired graft function and the development of renal insufficiency, other factors are, iron deficiency, inflammation, infection and immunosuppressive drugs (MMF, MPA, AZA, ACE-I, ABBs, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir. Vitamin B12 deficiency was reported to be the cause of PTA in 17–24%, Folic acid deficiency was the cause of anemia in 10%, acute kidney injury in 11.4% of cases, and acute rejection, accounting for 4% of cases. Infections were the cause of anemia in 19% of cases.
# Predictors of PTA included:
female sex, lower eGFR. Factors significantly associated with late PTA and a living donor as the transplantation source was protective.There was a strong association between Hb and graft function, elevated serum creatinine levels > 2 mg/dL, donor age (particularly above 60 years).
# Outcomes of Patients with PTA
# Mortality and Graft Failure
*Study showed that PTA at 12 months was associated with mortality and graft failure. *Prospective cohort study showed PTA to be associated with mortality and graft failure at the 4-year follow-up.
*In a large retrospective analysis it associated with mortality and graft failure at a median follow-up of 6 years.
*Other one reported that PTA at 12 months was associated with an increased risk of death, however, another retrospective conducted that, PTA after 3 months was associated with mortality and graft failure.
# Cardiovascular Morbidity
*A retrospective Canadian cohort study showed that anemia was an independent risk factor for LVH 1–5 years PKT that associated with a significant risk of death, while other conducted, adult renal transplant recipients who were free of cardiac disease 1 year PKT.
# GFR Decline
*Study, showed that anemia is associated with a decline of GFR and it is correction is associated with a reduction in the rate decline.
# Diagnostic Evaluation
*The diagnostic evaluation of renal transplant recipients is the same as non transplanted patients, i.e., red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferring saturation, serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when clinically indicated, In addition to test of medications (immunosuppressive and antimicrobial)
*Based on published evidence, a full anemia work-up approximately 3 months post transplantation is indicated as early recognition and treatment may improve the prognosis.
# Treatment of PTA
*Diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause.
*The target Hb level for treatment, followed by the type of treatment, i.e., erythropoiesis-
stimulating agents (ESA) and/or iron, should be determined.
*Anemia (Hb < 12.5 g/dL) was significantly associated with mortality in patients with and without ESA. In patients without ESA, a spontaneous rise in Hb was associated with decreased mortality at any level.
*In patients treated with ESA, improvement of anemia (Hb up to 12.5 g/dL) was associated with decreased mortality as well.
*Further increments in Hb levels led to a tendency toward increased rates of mortality, which became significant at Hb levels > 14 g/dL.
* Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR,and progression to ESRD and improved death-censored graft survival, significant improvement in quality of life, better cardiovascular outcomes, with no cardiac disorders (cardiac failure, arrhythmia, or myocardial infarction)
*The KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL.
*The(NKFKDOQI) guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/Dl.
*No specific recommendation was made for transplant recipients study suggest that the optimal target Hb level in KTR with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL.
*I.V. iron administration after transplantation increased Hb levels and reduced the eGFR decline
*If ESA is initiated, the iron status should be determined and iron stores should be repleted, as with CKD patients.
# What is the level of evidence provided by this article?
Level 5
# What is meant by the impact factor of a journal (please in your own words)?
*The impact factor (IF) is a measure of the frequency with which the average article in a journal has been cited in a particular year. It is used to measure the importance or rank of a journal by calculating the times its articles are cited.
How impact factor is calculated?
* The calculation is based on a two-year period and involves dividing the number of times articles were cited by the number of articles that are citable.
Zahid Nabi
2 years ago
This article by Gvili and Gafter has looked into the causes of anemia and it’s impact on kidney transplant patients.
Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation
Although successful kidney transplantation may correct anemia, up to 20–51% of patients remain anemic after transplantation at various time points
The authors have described anemia into early and late PTA.(late occurring 6 months after transplant)
Early PTA is usually due to iron deficiency. Iron deficiency may be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutritionIn in addition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
Interestingly one of the predictor of late onset PTA is early PTA.
Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies.
Folic acid deficiency was the cause of anemia in 10% of the cases in the study by this group which is a relatively low rate compared to the 23–41% reported in other studies.
Acute kidney injury and rejection along with infections have also been reported to be cause of PTA.
The authors have concluded by mentioning different studies that PTA is associated with increased mortality , LVH , increased CVS morbidity, decrease in GFR and worst graft outcomes.
The authors suggested that cause of anemia should be ascertained early and managed effectively to avoid its negative impact.
Target Hb in transplant patients should be between 12.5 -13 as shown by CARPIT study.
Level of Evidence is v
Impact factor of journal tells us the relative importance of that journal and it gives us the frequency with which average article in a journal has been cited in a particular time period
Abdul Rahim Khan
2 years ago
Briefly summarise this article Post transplant anaemia -PTA is an important entity with prevalence between 21-55%. Anaemia is defined as Haemoglobin <12 in females and <13 in males. Anaemia is associated with poor long term graft outcomes, left ventricular failure. Congestive cardiac failure and low eGFR. This article addresses PTA with prevalence aetiology, prognosis and management. Prevalence. Between 21-55% post transplant population. Early PTA Anaemia that occurs < 6 months post transplant. It is due to depleted iron stores pre transplant, peri operative losses, nutritional factors. Increased iron utilization by new onset erythropoiesis post transplant. Late PTA Anaemia that occurs > 6 months post transplant. This can lead to graft dysfunction . It is usually influenced by graft dysfunction. Other factors like iron deficiency, immune suppressants, ACEi,ARBs antibiotics like trimethoprim and sulphamethoxazole and antiviral may contribute. Predictors of late PTA cab be living donor, Use of ACEi, ARBi, donor age, infections, low eGFR, female sex PTA is associated with mortality and poor graft outcome Treatment of PTA Identification of underlying cause and then treat that. Iron replacement Erythropoiesis stimulating agents Aim to keep Hb above 12.5g/dl What is the level of evidence provided by this article? Review article Level V What is meant by the impact factor of a journal (please in your own words)? The impact factor is the tool to assess the importance f a journal and it is based on the number of citations to the article of this journal during specific time period. It calculated by ratio of the number of citations a journal receives in last 2years to the number of publications of that journal in last 2 years. Cites/doc (2 years). The article from a journal can used as citation in different books , dissertation and presentations. New journal will not have impact factor in first 2 years. So they may not have impact factor in first 2 years . This lead to bias .
Filipe prohaska Batista
2 years ago
This is a Narrative Review – Level 5
It is a paper discussing the causes of post-transplant anemia, specifically in kidney transplantation, dividing into early or late PTA. Another important discussion is the definition of target hemoglobin levels between 12.5 and 13 g/dL.
Early PTA (in the first six months after transplantation) is closely related to iron deficiency. Risk factors include donor age (particularly over 60 years), use of ACE inhibitors or angiotensin receptor blockers, recent infection, or use of immunosuppressants such as MMF and Azathioprine.
Late PTA has early PTA as one of the risk factors, but in these cases, there is an association with kidney injury and graft loss. There are several studies also correlating mortality, but still with conflicting data. However, the impact of anemia on the graft is indisputable. Other deficiencies should be investigated (vitamin B12, folic acid, and nutritional deficiencies).
Cardiovascular morbidity is increased in patients with post-transplant anemia for several reasons, being an independent risk factor for congestive heart failure. Over time, there is a decrease in Creatinine Clearance and consequent loss of the graft.
Treatment is the diagnosis and treatment of all reversible causes (mainly those related to the patient’s nutrition). Erythropoietin stimulators have a well-defined role in the literature, with data showing an improvement in the quality of life of individuals who achieve target hemoglobin. Iron replacement, whether oral or intravenous, plays a crucial role.
The Impact Factor is calculated by dividing the number of citations in the journal citation report per year by the total number of articles published in the two previous years.
Nahla Allam
2 years ago
Summary :
Definition :
Post transplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation
PTA is not defined uniformly either timing after transplantation or in terms of the degree of anemia:
Early PTA (up to 6 months after transplantation).
Late PTA (after six months)
Anemia in most studies is defined as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men, following World Health Organization (WHO) criteria and the American Society of Transplantation.
Causes of and Predictive Factors for PTA:
Ø Early PTA is usually due to:
1. Iron deficiency
2. Inadequate iron stores at the time of transplantation
3. blood loss during surgery
4. increased iron utilization with the onset of erythropoiesis
5. poor nutrition.
Ø Late PTA is usually due to:
1. iron deficiency
2. inflammation
3. infection
4. immunosuppressive medications
ü Other causes:
Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia.
Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies.
The folic acid deficiency was the cause of anemia in 10% of the cases
Other reasons for PTA included acute kidney injury, acute rejection, and Infections.
üPredictors of PTA:
Factors associated with early PTA included: female sex, lower eGFR, and hypochromic red blood cells
Elevated serum creatinine levels > 2 mg/dL were associated with late PTA.
1-Donor aged above 60 years
2- ACE inhibitors or angiotensin receptor blockers,
3- immunosuppressive drugs such as mycophenolate mofetil and azathioprine,
4- recent infection.
ü Outcomes of Patients with PTA:
1. Mortality and Graft Failure
2. Cardiovascular Morbidity
3. GFR Decline
ü Diagnostic Evaluation:
ü The diagnostic evaluation of renal transplant recipients should include an assessment for “the usual” causes of anemia as with non-transplanted patients
4. tests for the presence of hemolysis (haptoglobin
5. lactate dehydrogenase, and indirect bilirubin
ü Specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial
Treatment of PTA:
ü The management of PTA starts with diagnosing and treating all reversible causes, as therapy should be directed at the underlying cause. However, there is no specific recommendation for treating kidney transplant recipients.
ü Most importantly, the target Hb level followed by the type of treatment, i.e., erythropoiesis-stimulating agents (ESA) and iron, should be determined.
ü The KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL. The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative and targeting (NKFKDOQI) guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/ dL. But, again, no specific recommendation was made for transplant recipients.
· Level 2.
· Impact factor for journal:
The journal impact factor is the number of articles published in the past two years.the impact factor is calculated by dividing the number of citations in the year by the total number of articles published in the two previous years
Impact factors are used to measure the importance of a journal by calculating the number of times selected articles are cited within the last few years.
Sahar elkharraz
2 years ago
Post transplant anemia:
Definition of anemia in women less than 12g/dl and male less than 14g/dl.
Early PTA is within 6 months
Late PTA is more than 6 months.
Prevalence of anemia is 20-51% in post transplant.
Early PTA causes mainly IDA results from depletion of iron store before transplant.
Peri operative blood loss
Poor nutrition
Causes of late PTA:
IDA
infection
immunosuppressive drug
Post transplant anemia assess with decrease graft function and decline eGFR and left ventricle hypertrophy and congestive heart failure.
Predictor of late PTA:
early PTA
serum creatinine level more than 2mg/dl
Age more than 60y
Medication like ACEI / ARBS/ azathioprine and septrin and valgancyclovir
Aetiology and incidence according to retrospective study done between 2000-2016 in rabin medical center.
IDA 13%
nutritional deficiency
Vit B12 deficiency 17-24%
Folic acid deficiency 10%
AKI 11.4%
Acute rejection 4%
Infection 19%.
Outcome of patients with PTA:
Anemia associated with graft loss and progressive decline in eGFR.
There’s no evidence of anemia increase mortality but it’s depend on severity of anemia.
Anemia is independent risk of LVH and de novo congestive heart failure.
Diagnosis of PTA:
RBC indices
Reticulocyte count
S.iron / TIBC/ ISR/ S. ferritin , folate and vit B12.
S. haptoglobin , LDH, indirect bilirubin.
Evaluation of medication: Immunosuppressive therapy and antimicrobial agents contribute to anemia.
So early recognition and early treatment improve graft function.
Management:
Treatment of underlying cause
Intravenous iron
ESA
What is the level of evidence provided by this article?
Level V
What is meant by the impact factor of a journal (please in your own words)?
The average number of citations published in journal within previous 2 years
Amit Sharma
2 years ago
Briefly summarise this article
Anemia is defined as haemoglobin less than 12 g/dl in women and <13 g/dl in men. Kidney transplant patients develop post-transplant anemia (PTA) with the incidence rates ranging from 20% to 51%. Early PTA (within 6 months post-transplant) occurs in upto 50% while the incidence of late PTA ranges from 23-35%. PTA has been shown to be associated with increased rates of all-cause mortality, graft failure, congestive cardiac failure, left ventricular hypertrophy and fall in GFR.
Early PTA is usually caused due to iron deficiency while late PTA is caused due to reduced graft function, iron deficiency, vitamin B12 and folic acid deficiency, inflammation, infection, and medications including immunosuppressants (like MMF and azathioprine), ACE inhibitors, Angiotensin receptor blockers, trimethoprime-sulfamethoxazole and ganciclovir. Other causes of PTA include AKI and acute rejection. Predictors of PTA include recent infection, donor age more than 60 years, use of ACE inhibitors and ARBS, MMF and azathioprine. Predictors specific for early PTA include female gender, lower GFR and hypochromic RBCs. Predictors for late PTA include early PTA, non-living donor, female gender and increased serum creatinine at 3-month post-transplant.
Studies analysing outcomes with PTA with respect to mortality show increase in mortality by 69%, more with severe anemia (hemoglobin<11 g/dl). This increase is not seen with mild anemia. The incidence of graft failure increases by 2.46 times and GFR falls by 5.26 ml/min/1.73m2 between 6 and 24 months post-transplant. PTA is associated with increased left ventricular hypertrophy and CCF leading to increased mortality.
The diagnostic evaluation of PTA involves a full anemia work-up at 3 months post-transplant including RBC indices, reticulocyte count, peripheral blood film, serum iron, TIBC, ferritin and transferrin saturation, serum vitamin B12, folic acid and haptoglobulin levels.
Management of PTA includes diagnosis and treatment of all reversible causes of anemia. Hemoglobin <12.5 g/dl has been shown to be associated with increased mortality. Correction of PTA using erythropoietin has been shown be associated with better graft survival and quality of life (CAPRTI trial). Similar correction of anemia in CKD patients has not shown delay in progressive renal failure and has been shown to be associated with increased cardiovascular events (CHOIR and TREAT trial).
Based on these data, KDIGO recommends use of erythropoietins in CKD only if hemoglobin is less than 10 with target of 11.5g/dl. Optimal target hemoglobin in kidney transplant recipients is 12-13g/dl. Intravenous iron use in transplant recipients has been shown to increase hemoglobin levels and decrease the eGFR fall. Iron stores should be replenished before starting erythropoietins. In early PTA management, both oral and intravenous irons are equally efficacious with respect to time required to achieve hemoglobin of more than 11g/dl. Intravenous iron use is safe in transplant recipients.
What is the level of evidence provided by this article?
The level of evidence is Level 5 – narrative review.
What is meant by the impact factor of a journal (please in your own words)?
Impact factor of a journal is the average number of citations received by each article published in that journal in the previous 2 years. It is a number derived by dividing the total number of citations received by total number of articles published in the journal.
Reference:
Sharma M, Sarin A, Gupta P, Sachdeva S, Desai AV. Journal impact factor: its use, significance and limitations. World J Nucl Med. 2014 May;13(2):146. doi: 10.4103/1450-1147.139151. PMID: 25191134; PMCID: PMC4150161.
Muntasir Mohammed
2 years ago
IV. Posttransplantation Anemia in Kidney Transplant Recipients
Briefly summarise this article
Introduction
Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation. It has been shown to be negatively associated with:
1. Increased rates of all cause mortality.
2. Graft failure
3. Congestive heart failure.
4. Left ventricular hypertrophy.
5. Decline in the estimated glomerular filtration rate (eGFR).
Prevalence and Epidemiology
Although successful kidney transplantation may correct anemia, up to 20–51% of patients remain anemic after transplantation at various time points.
Two main types:
1. Early PTA (up to 6 months after transplantation), occurs in 50% of cases.
2. Late PTA (after 6 months), occurs in 23-35%.
Defined as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men, in accordance with World Health Organization (WHO) criteria and the American Society of Transplantation.
Causes of and Predictive Factors for PTA
1-Early PTA is usually due to iron deficiency.
2-ate PTA has been associated with impaired graft function
and the development of renal insufficiency. Late PTA is predominantly influenced by a reduced allograft function. However, other factors, i.e., iron deficiency, inflammation and infection, immunosuppressive medications (Mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia
Predictors of PTA
In retrospective study, predictors of early PTA included:
· Female sex.
· Lower eGFR.
· Hypochromic red blood cells
Factors significantly associated with late PTA (2 years after transplantation) included:
· Early PTA, (HR 0.601; 95% CI 0.453–0.799, for every
· Living donor as the transplantation source was protective
· Donor age (particularly above 60 years).
· Use of ACE inhibitors or angiotensin receptor blockers.
· Use of immunosuppressive drugs such as mycophenolate mofetil and azathioprine.
· Recent infection.
Etiology of PTA
· Iron deficiency is the most common contributing factor for early PTA.
Reasons for that include:
1. Inadequate iron stores at the time of transplantation.
2. Blood loss during surgery.
3. Increased iron utilization with the onset of erythropoiesis.
4. Poor nutrition
· Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies.
· Folic acid deficiency was the cause of anemia in 23-41%
· Acute kidney injury, accounting for 11.4% of cases, and
· Acute rejection, accounting for 4% of cases.
· Infections were the cause of anemia in 19% of cases.
Outcomes of Patients with PTA Mortality and Graft Failure
PTA has previously been shown to be associated with the composite outcome of all-cause mortality and graft loss. However, while almost all of the studies have shown a significant correlation with graft failure, results regarding the association between anemia and mortality are inconsistent..
Cardiovascular Morbidity
Anemia was identified as an independent risk factor for de novo congestive
heart failure and left ventricular hypertrophy in retrospective studies. GFR Decline
Anemia is associated with a decline of GFR and correction of anemia is associated with a reduction in the rate decline.
Diagnostic Evaluation
The diagnostic evaluation of renal transplant recipients should include an assessment of :
1. The usual” causes of anemia as with nontransplanted patients.
Red blood cell indices,
Reticulocyte counts
Serum iron, total iron-binding capacity (transferrin), percent transferrin
saturation, serum ferritin.
Folate
Vitamin B12
Tests for presence of hemolysis (haptoglobin) when
clinically indicated (elevated reticulocyte counts, lactate
dehydrogenase, and indirect bilirubin).
2. Specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc., should be sought.
Treatment of PTA
Treatment should be directed at the underlying cause. However,
there is no specific recommendation for the treatment of kidney transplant recipients. Questions to be addressed are target Hb and weather to give and /or ESA.
Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD and improved death-censored graft survival. Compared to the partial-correction group, the complete-correction group had a smaller decrease in the estimated creatinine clearance (i.e., 5.9 vs. 2.4 mL/
min/1.73 m2), a lower rate of ESRD (i.e., 21 vs. 4.8%), and a higher death-censored graft survival (i.e., 80 vs. 95%). There was also a significant improvement in quality of life in the full-correction group. Regarding cardiovascular outcomes, although the numbers were small, there were no cardiac disorders (cardiac failure, arrhythmia, or myocardial infarction) in the full-correction group compared to 4 patients (8%) in the partial-correction group,
In conclusion, PTA is a common complication of renal transplant recipients. It is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anemia. Treatment of PTA should begin as soon as possible after kidney transplantation. Based on data derived from the CAPRIT study and the observational study by Heinze et al, it appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
What is the level of evidence provided by this article?
This is a review article level 4.
What is meant by the impact factor of a journal (please in your own words)?
Impact factor (IF) is used to assess the relative importance of a journal within its field and to measure the frequency with which the “average article” in a journal has been cited in a particular time period. Journal which publishes more review articles will get highest IFs.Impact factor can’t be calculated for journal unless it completes 3 years of publications. The problems with IF, it reflects the number of citations which may not always reflect how good is the journal. Second thing journal which publishes more review articles will get high IF and journal which publishes more original articles, which may be landmarks in the field may get lower IF. Lastly IF reflects 2 years only of the journal not the whole duration of its life. Formula of IF = total citations of all articles in previous 2years/number of articles published in same 2years period
Mohamad Habli
2 years ago
Briefly summarize this article
According to WHO and AST, anemia is defined as hemoglobin levels < 12 g/dL in women and < 13 g/dL in men.
Two types of anemia are recognized post-transplantation
– Early post-transnsplanty anemia- up to 6 months after transplantation, prevalence is about 50% according to various studies. It is usually caused by iron deficiency from blood loss during surgery or delay graft function.
– Late PTA after 6 months- with prevalence of 23–35%. Usually due to progressive decline in kidney function- chronic allograft nephropathy. PTA is associated with increased risk of cardiovascular mortality and worsening of kidney function.
Etiology of PTA:
Iron deficiency is the most common cause of PTA in the early post-transplantation period. Low iron stores post-operatively is linked to blood loss during surgery, poor nutrition and inflammatory state which decreases utilization of iron into bone marrow.
Vitamin B12 deficiency
Folic acid deficiency
AKI
Acute rejection,
Infections
Outcomes of Patients with PTA
Mortality and Graft Failure
PTA was shown to be associated with increased all-cause mortality and graft loss, as reported in some studies. However, other studies fail to show an association with mortality risk, but a significant association with graft loss was demonstrated. Anemia is an independent risk factor for LVH and heart failure.Anemia is associated with worsening of kidney function, and correction of anemia is associated with a reduction in the rate decline.
Diagnostic Evaluation
RBC indices, Retic counts, serum iron, TIBC, Ferritin, vitamin B12, folic acid, hemolytic workup and stool occult blood gor GI losses
Treatment of PTA
Treatment should be focused on the underlying reversible causes.
KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL.
The optimal target of Hb in kidney transplant recipients was suggested to be 12-13 g/dl .
What is the level of evidence provided by this article?
Level 2
What is meant by the impact factor of a journal (please in your own words)?
Impact factor is calculated by dividing the number of citations of the journal by the the sum of its citable publications during the previous two consecutive years.
Wael Jebur
2 years ago
Post transplant anemia PTA is commonly encountered in our daily practice. This article, elaborately discussed the subject, detailing its etiology, causes, classification, risk factors, outcome and comparing different studies conducted to address this issue.
definition of anemia :
HB below 13 in male and below 12 in female.
Early PTA , diagnosed within 6 months post transplantation, incidence around 50 %.
Late PTA anemia diagnosed after 6 months of kidney transplantation.
Etiology:
Most common cause of early PTA is Iron deficiency secondary to pretransplant depletion of Iron store, peri-transplant blood loss and the escalating endogenous level of allograft produced Erythropoietin consuming the matched iron store.
Risk factors:
female patients, low GFR, iron store.
For late PTA main risk factors are Iron deficiency anemia, GFR, life donor vs cadaveric donors, chronic kidney disease and allograft failure.
Furthermore, medications related, mainly MMF, valgancyclovir, TMS, CNI, and Renin inhibitors like ACEi.
Several studies were reviewed, showcasing the argumantative impact of anemia on mortality rate and progression of allograft failure, highlighting the debate on this contentious issue, Increased mortality was attributed to LVH.
Treatment was directed towards the underlying etiological factor, basically Iron replacement and ESA therapy. with target HB depend on GFR and the presence of allograft dysfunction.
however, it was not clear what is the indication to start ESA post transplantation as there is no consensus on this issue. Nevertheless, extrapolating the recommendation of KDOGI guideline on the time and threshold for initiating iron and ESA therapy.
I have published a case report discussing the same issue few years back , I am sharing here with you.
The level of evidence is 4 as its a narrative paper.
Impact factor: in my humble language and understanding it is how popular and well known is the journal with how many subscribers and citations made over a period of time
Khadija Alshehabi
2 years ago
Briefly summarise this article
Post-transplantation anemia (PTA) is common among kidney-transplant patients. There is the early PTA which is (up to 6 months after transplantation) with a prevalence of around 50% and late PTA (after 6 months) with around 23-35%. Causes of PTA
Early PTA:
Iron deficiency is the most common contributing factor for early PTA
Inadequate iron stores at the time of transplantation blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition all contribute to the occurrence of iron deficiency
Late PTA:
Can appear as late as up to 8 years. Late
PTA is predominantly influenced by a reduced allograft function.
Other factors:
iron deficiency
inflammation and infection
Medications: immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin- aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir. Other Causes for PTA:
Vitamin B12 deficiency
Folic acid deficiency
Acute kidney injury
Acute rejection
Predictors of PTA
female sex
lower eGFR
Hypochromic red blood cells
Early PTA (for the late PTA)
a living donor
donor age > 60
Medications: ACEi or ARBs MMF and azathioprine
Recent Infection
a recent infection.
early PTA is a predictor of late PTA
Outcomes of Patients with PTA
· Mortality and Graft Failure
PTA has previously been shown to be associated with the composite outcome of all-cause mortality and graft loss, though results about mortality are inconsistent.
However, overall, in certain studies. the association between anemia and mortality was related to severity. Severe anemia (Hb <11 g/dL) was consistently associated with mortality while mild anemia was not. Both severe and mild anemia were associated with graft failure.
· Cardiovascular Morbidity
Anemia is considered as an independent risk factor for left ventricular hypertrophy & de novo congestive heart failure.
· GFR Decline
Anemia is associated with a decline of GFR and correction of anemia is associated with a reduction in the rate decline.
Diagnostic Evaluation
· red blood cell indices
· reticulocyte counts
· serum iron, total iron-binding capacity, transferrin saturation
· serum ferritin, folate, and vitamin B12
· haptoglobin
· lactate dehydrogenase
· Indirect bilirubin
In addition, potential causes of anemia should be sought.
Treatment of PTA
Treatment should be directed at the underlying cause
Erythropoiesis-stimulating agents (ESA) and/or iron, should be determined.
KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is <10.0 g/dL, with a target Hb level of 11.5 g/dL based on landmark trials (CHOIR, TREAT, CREATE).
The CAPRIT trial, however, which was done in transplanted patients is smaller than all of previous trials and it is also limited by its short duration of 2 years. Nevertheless, it is the only randomized controlled trial (RCT) addressing this question in the transplanted population.
The results of this study as well as those of another large observational study suggest that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL.
It seems reasonable to treat with ESA and/or IV iron if indicated in transplanted patients.
What is the level of evidence provided by this article?
Evidence from systematic reviews of descriptive and qualitative studies (meta-synthesis).
What is meant by the impact factor of a journal (please in your own words)?
It is a measure to evaluate the importance of a journal within its field and this can be assessed by the number of its citations over a 2-year period.
It can be calculated after completing the minimum of 3 years of publication. Therefore, impact factor cannot be calculated for new journals.
The disadvantage is the misuse in evaluating individuals is it depend upon personal judgments.
Dr. Tufayel Chowdhury
2 years ago
Post transplant anemia is a common complication of renal transplant recipients. Prevalence is 20- 50% at various time points after transplantation.
PTA is associated with increased mortality, reduced graft survival and a decline GFR.
Anemia is defined as Hb level <12 g/dl in women and <13g/dl in men.
Early PTA is defined as anemia which develops upto 6 months after transplantation and late PTA is defined as anemia which develops after 6 months.
Causes
Early PTA is usually due to iron defeciency.
Late PTA has been associated with impaired graft function and the development of renal insuffiency. Hoever other factors like iron defeciency, inflammation,infection, immunosuppressive medications, ACE inhibitors, ARB, trimethoprim – sulfamethoxazol and anti viral agents ganciclovir may causes anaemia.
Diagnostic evaluation:
Red cell indices, reticulocyte counts, s iron, TIBC, s. ferritin, folate, vitamin B 12, and tests for hemolysis when indicated.
Management
Starts with diagnosis and treatment of all reversible causesBased on data from CAPRIT is upto 12. 5 to 13 g/dl. Appropriate treatment withESA i.v iron should be given
Tahani Ashmaig
2 years ago
☆ Summary: Posttransplantation Anemia in Kidney Transplant Recipients (KTR)
▪︎This review provided updated information about the prevalence of PTA in KTR and the causative and predictive factors.The effect of anemia on long-term outcomes & treatment options.
▪︎Introduction Post-transplantation anemia (PTA) is common among KTR & is negatively associated with the following long-term outcomes: increase mortality rate, graft dysfuction, congestive heart failure, LVH, and a decline in the (eGFR).
▪︎Prevalence: – Up to 20–51% of patients remain anemic at various time points post transplantation. – Two types of PTA are distinguished early (up to 6 months after transplant with prevalence about 50%) and late (after 6 months in 23–35%). ▪︎Predictors of PTA – Female sex, lower eGFR, and hypochromic red blood cells. – Factors significantly associated with late PTA (2 years after transplantation) included early PTA, and a living donor. TRESAM showed a strong association between Hb and graft function; Elevated serum creatinine levels >2 mg/dL were associated with late PTA. – Other factors that were associated with PTA included: donor age (particularly above 60 years), the use of ACE I or ARB, the use of immunosuppressive drugs such as MMF & azathioprine, and a recent infection. – The observation that early PTA is a predictor of late PTA. Etiology of PTA – Iron deficiency is the most common contributing factor for early and late PTA due to: inadequate iron stores at the time of transplantation, blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition. – Common causes of late PTA were nutritional deficiencies (Iron &Vitamin B12, Folic acid) – Other causes of PTA: acute kidney injury, acute rejection and infections. Outcomes of Patients with PTA: 1. Mortality & Graft Failure. 2. Cardiovascular Morbidity (LVH & CHF). 3. GFR Decline Diagnostic Evaluation – Should include: an assessment for “the usual” causes of anemia. In addition to, specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications, concurrent infections, etc., – Early recognition & treatment may improve the prognosis. Treatment of PTA – Should be directed to the underlying cause. – There is no specific recommendation for the treatment of kidney transplant recipients. – Treatment should target Hb level, followed by the type of treatment, i.e., erythropoiesis-stimulating agents and/or iron, should be determined. – A study showed that: normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β can reduce the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD, improved graft survival, improvement in quality of life and no cardiac disorders. – The KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is <10.0 g/dL, with a target Hb level of 11.5 g/dL. – The NKFKDOQI guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/ dL. – The optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL ( according to CAPRIT trial and large observational study by Heinze et al). – Iron deficiency, even without anemia, has been shown to be an independent predictor of mortality in KTR. However, i.v. iron administration after transplantation increased Hb levels and reduced the eGFR decline. – If ESA is initiated, the iron status should be determined and iron stores should be repleted, as with CKD patients. – It is unclear in the transplant setting whether i.v. iron is better than orally administered iron. But according to study results, it seems reasonable to treat transplanted patients with i.v. iron. Conclusion – PTA is associated with reduced mortality (which is related to severity of anaemia), reduced graft survival, and a decline in GFR. – Treatment of PTA should begin as soon as possible after renal transplantation. – Based on data derived from the CAPRIT and study and the observational study by Heinze et al., it appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. To reach this target, appropriate treatment with ESA and i.v. iron should be given.
_______ ☆What is meant by the impact factor of a journal (please in your own words)? It means the relative importance of a journal within its field and to measure the frequency with which the average article in a journal has been Cite in a particular time period.
Mahmoud Wadi
2 years ago
Briefly summarise this article
Introduction
– Post transplantation anemia (PTA) is common among
kidney-transplant patients.
-A prevalence of 20-51% after transplantation.
– Early PTA is anemia usually develops up to 6 months after transplantation, and late anemia which develops after month.
– PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR and association with mortality is related to the severity of the anemia and to specific causes of anemia.
-The following long-term outcomes: –
*increased rates of all-cause mortality , graft failure , conges tive heart failure , left ventricular hypertrophy ,
and a decline in the estimated glomerular filtration rate (eGFR) .
– The optimal target hemoglobin level in kidney transplant recipients up to 12.5–13 g/dL.
Prevalence and Epidemiology
-Although successful kidney transplantation may correct anemia, up to 20–51% of patients remain anemic after transplantation at various time points.
-Anemia in most studies is defined as hemoglobin (Hb)
levels < 12 g/dL in women and < 13 g/dL in men, in accor-dance with World Health Organization (WHO) criteria
and the American Society of Transplantation.
– The prevalence of early PTA is about 50% and 23-35% late PTA.
Causes of and Predictive Factors for PTA
–
-Early PTA is usually due to iron deficiency.
– Late PTA is usually defined as anemia that occurs
more than 6 months after transplantation, and it can ap-
pear as late as up to 8 years later.
-late PTA has been associated with impaired graft func-
tion and the development of renal insufficiency.
– Late PTA is predominantly influenced by a reduce allograft
function.
– Other factors, include iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia .
Etiology of PTA
The most common contributing factor for early PTA:- 1- Iron deficiency (34.7%) 2- Inadequate iron stores at the time of transplantation 3- Blood loss during surgery 4- Increased iron utilization with the onset of erythropoiesis 5- And poor nutrition all contribute to the occurrence of iron deficiency. 6- 61% late PAT (poor nutrition)
7- Vitamin B12 deficiency was cause of PTA in 17–24% .
8- Folic acid deficiency was the cause of anemia in 10%
Outcomes of Patients with PTA
1- Mortality and Graft Failure
2- Cardiovascular Morbidity
3- GFR Decline
-A retrospective multicenter analysis using aFrench database that included 4,217 transplant recipients.
-showed that PTA at 12 months was associated with mortality and graft failure.
– A retrospective multicenter analysis using a French database that included 4,217 transplant recipients.
– A prospective cohort study of 938 kidney transplant recipients in Hungary showed PTA to be associated with mortality and graft failure at the4-year followup.
-In a large retrospective analysis of 2,031 transplant recipients in Austria, anemia was significantly associated with mortality and graft failure at a median follow-up of 6 years – A retrospective series of 626 transplant recipients in Pennsylvania, USA, reported that PTA at 12 months.
IN all of these studies PTA was significantly assaciated with mortality and graft loss .
–In the other study , the association between anemia and mortality was related to severity.
–Severe anemia (Hb < 11 g/dL) was consistently associated with mortality, while mild anemia was not.
–Both severe and mild anemia were associated with graft failure.
Diagnostic Evaluation
The diagnostic evaluation of renal transplant recipients should include:
– Red blood cell indices,
-Reticulocyte counts,
– Serum iron, TIBC
-TSAT%,
-Serum ferritin,
-Folate, and vitamin B 12
-Thyroid function tests – And hemolysis (haptoglobin) when (elevated reticulocyte counts, lactaedehydrogenase, and indirect bilirubin).
Treatment of PTA
1- The management of PTA starts with diagnosis and
treatment of all reversible causes.
2-Treatment should be directed at the underlying cause.
3-There is no specific recommendation for the treatment of
kidney transplant recipients .
4- Most importantly, the target Hb level for treatment, followed by the type of treatment, i.e., (ESA) and/or iron, should be determined.
5- In the CAPRIT trial mentioned above higher Hb levels were associated with graft survival and in this trial, 125 renal transplant recipients were randomly assigned to re-
ceiving epoetin-β with a target of 13–15 g/dL (complete correction group) or 10.5–11.5 g/dL (partial correctio group).
6- Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR,and progression to ESRD and improved death-censored graft survival.
7-The optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL.
8- In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
Conclusion
PTA is a common complication of renal transplant recipients associated with reduced mortality, reduced graft survival, and a decline in GFR.
Treatment of PTA should begin as soon as possible after kidney transplantation.
CAPRIT study and the observational study by Heinze et al. it appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL.
In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
· What is the level of evidence provided by this article?
The level V
· What is meant by the impact factor of a journal (please in your own words)?
Impact factor of a journal = Total number of times its articales were cited during the two previous years ÷ Total number of citable articales in the journal during those two years.
Huda Saadeddin
2 years ago
Posttransplantation anemia (PTA) is common among kidney transplant patients.
divided into two types
Early PTA is usually defined as anemia which develops up to 6 months after transplantation
late PTA is defined as anemia which develops after 6 months up to 8 years
optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL.
Prevalence and Epidemiology
up to 20–51% of patients remain anemic after transplantation.
The prevalence of early PTA is about 50% and the prevalence of late PTA declines to about 23–35% at various time points up until 8 years after transplantation.
Causes of and Predictive Factors for PTA
Early PTA
iron deficiency >>>
depletion of iron stores before transplantation
perioperative blood loss
poor nutrition
increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia
late PTA
impaired graft function and the development of renal insufficiency factors
Treatment
there is no specific recommendation for the treatment of kidney transplant recipients
Most importantly, the target Hb level for treatment, followed by the type of treatment, i.e., erythropoiesis-stimulating agents (ESA) and/or iron, should be determined.
In the CAPRIT trial mentioned abovehigher Hb levels were associated with graft survival.
Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD and improved death-censored graft survival.
If ESA is initiated, the iron status should be determined and iron stores should be repleted, as with CKD patients.
It appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
What is the level of evidence provided by this article? level of evidence V
What is meant by the impact factor of a journal ¿ Impact factor is commonly used to evaluate the relative importance of a journal within its field and to measure the frequency with which the “average article” in a journal has been cited in a particular time period.
Mu'taz Saleh
2 years ago
Post transplantation anemia (PTA) is common among kidney transplant patients.
1- Early PTA : anemia which develops up to 6 months after transplantation
2- Late PTA : anemia which develops after 6 months
The prevalence of early PTA is about 50% and the prevalence of late
PTA declines to about 23–35% at various time points up until 8 years after transplantation
PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR.
Treatment of PTA should probably begin as soon as possible after kidney transplantation
The optimal target hemoglobin level in kidney transplant recipients should be up to 12.5–13 g/dL.
Causes of PTA :
1- Early : Iron deficiency anemia
depletion of iron stores before transplantation,
perioperative blood loss,
poor nutrition
increased iron utilization with the onset of erythropoiesis
2- Late :
associated with impaired graft functionand the development of renal insufficiency
The management of PTA starts with diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause with HGB level of 12.2 – 13 . However, there is no specific recommendation for the treatment of kidney transplant recipients
What is the level of evidence provided by this article?
level of evidence V.
What is meant by the impact factor of a journal (please in your own words)?
The impact factor of a journal in a period of time means how many citations in a given period of time to number of citable articles in the journal, journals with high impact factor more stronger than those with low one.
thanks
saja Mohammed
2 years ago
Summarize the article Introduction
Anemia post kidney transplantation is common and varies in prevalence between 20-51%at different points times (1-4).
Post kidney transplant anemia (PTA) can be classified as early PTA in the first 6 months which could be multifactorial including IDA,
Late PTA after 6 months which usually associated with graft dysfunction, infection, rejection, malignancy, and drug effect. According to the WHO criteria and American transplant criteria, anemia is defined by a low HB level of < 12 gm in females, and < 13 gm in males Early PTA is more prevalent and reported up to 50% as per the evidence from many studies, its more of IDA due to surgical blood loss and depletion of the iron store, poor nutrition pre-transplantation period also due to increased iron utilization with increased erythropoiesis. While late PTA in the range of 23-35% in different time points up to 8 years after transplantation, usually associated with reduced graft function, infection, inflammation with IDA, drug effects like MMF, AZATHIOPRINE, ACEI, ARBS, antibiotics like trimethoprim and antiviral like ganciclovir. Early PTA is the most prognosticator of late PTA, PTA is associated with higher mortality and morbidity. The more severe degree and type of anemia can affect the graft function with reduced GFR and lower survival rate, so anemia post-transplantation should be addressed and treated promptly with epoetin (ESA) and iron supplement, targeting a higher level of HB in the range of 12-13gm.
Predictors for PTA: Early PTA
1. Female sex
2. Lower GFR
3. percentage of hypochromic RBCs Late PTA
1. Early PTA
2. Living donor source for KTX was protective
3. donor age > 60 years
4. use of ACEI, ARBS, MMF, azathioprine
5. recent infection AIM of this study
1- To give an update on the prevalence of PTA
2- Determine the risk factors
3- Address the mortality and morbidity of PTA
4- Determine the PTA effect on long-term outcome
5- Debate treatment opportunities Method and setting of this study:
a large retrospective cohort from a single tertiary center in Israel (RMC) included > 1135 KTX recipients with 4 years FU.
Period of the study 2002-2016 Results:
Prevalence of PTA of 36%, and IDA due to nutritional deficiency contribute to most of the causes of early PTA
AKI in 11.3 %, acute rejection in 4%, infection in 19%, lower rate of folic acid deficiency was found in 10% (compared to 23-41% in other studies)
PTA is associated with reduced GFR by 2.6ml/min/1.73m2, similar to finding in other studies like CARPET Trails, and correction of anemia prevents GFR decline rate.
The majority of studies from a diverse population show conflicting results regarding the PTA and the mortality risk however majority confirm the association between PTA and graft failure. Only severe anemia was associated with increased HR of mortality while mild and severe anemia were both associated with graft failure in this cohort study and this might explain the conflicting results from other studies. Cardiovascular morbidity
Again, PTA is associated with increased cardiovascular risk, and based on many studies PTA consider an independent risk of LVH, LVF, and cardiac death Management of PTA
The investigation includes the same approach for anemia work up, in general, including the RBCs indices and iron profile transferrin binding, IBC, and ferritin, in certain conditions will do hemolytic markers like LDH, PERIPHERAL SMEAR, indirect bilirubin, and haptoglobin, B12, Folate, viral infection screen like CMV, EBV, parvoviral 19
Early treatment of PTA by targeting the underlying cause and use of iron replacement and ESA with target higher level of HB 12.5-13gm based on data from CARPET trial and Heinz et al observational study.
What is the level of evidence provided by this article?
retrospective cohort study level 111
What is meant by the impact factor of a journal (please in your own words)?
impact factor is an indicator used to measure the impact of the journal based on the calculation of the total number of cited articles per year divided by the number of publications in two years’ time.
Mohamed Mohamed
2 years ago
IV. Posttransplantation Anemia in Kidney Transplant Recipients Briefly summarise this article Definitions
Early PTA: up to 6 months post transplantation
Late PTA: after 6 months
Anemia (WHO & the AST definition):
Hb <12 g/dL in women & < 13 g/dL in men. Prevalence
Early PTA: 50%
Late PTA: 23–35% Causes: Early PTA is due to iron deficiency (ID).ID is due to depletion of iron stores before transplantation, perioperative blood loss, poor nutrition, & increased iron utilization with the onset of erythropoiesis with increasing levels of the newly graft-produced erythropoietin.
Late PTA is usually associated with impaired graft function & the development of renal insufficiency. Other factors include: ID, inflammation & infection, IS medications
(MMF, MPA, & azathioprione),RAS blockers, & antimicrobials (e.g. septrin & ganciclovir)
Vitamin B12 deficiency causes PTA in 17–24% of patients.Folic acid deficiency is responsible for 10% of cases of PTA.
Other causes include AKI & acute rejection. Predictors of PTA
Include:
Female sex
Early PTA is a predictor of late PTA.
A living donor as the transplantation source is protective.
There is a strong association between Hb & graft function. Elevated creatinine levels
> 2 mg/dL are associated with late PTA.
Donor age (particularly above 60 years) Outcomes of Patients with PTA Mortality & Graft Failure
PTA at 12 months was associated with mortality & graft failure (French database, 4,217 transplant recipients).
PTA associated with mortality & graft failure at the 4-year follow-up (A prospective cohort study of 938 recipients in Hungary).
Anemia was significantly associated with mortality & graft failure at a median follow-up of 6 years(a large retrospective of 2,031 recipients in Austria).
PTA at 12 months was associated with an increased risk of death (A retrospective of 626 recipients in Pennsylvania, USA, reported that).
PTA after 3 months was associated with mortality & graft failure (retrospective of 1,023 recipients in Chicago, IL, USA).
The authors showed that PTA was associated with increased mortality at 2 years in 266 transplant recipients.
In a more recent study of 1,139 patients, PTA at any time point (6–18 months after transplantation) was associated with the composite endpoint of mortality & graft failure, as well as with each of the components.
In a retrospective European study of 825 recipients, PTA was not associated with all-cause mortality with a follow-up of 8 years.
Hb levels were not associated with any effect on cardiovascular morbidity or mortality at a 5- to 6-year follow-up (cohort of 2,102 Danish transplant recipients).
PTA at 12 months was not associated with mortality (a retrospective Chinese study of 887 recipients,).
In all of these studies anemia was significantly associated with graft loss.
Other studies failed to show an association with all-cause mortality, but a significant association with graft loss was reported.
The author reported that severe anemia
(Hb < 11 g/dL) was consistently associated with mortality, while mild anemia was not. Both severe & mild anemia were associated with graft failure.
Cardiovascular Morbidity
Anemia is an independent risk factor for LVH 1–5 years after transplantation (Canadian cohort of 473 recipients). LVH & anemia were associated with a significant risk of death.
Anemia was an independent risk factor for de novo CHF in another retrospective Canadian cohort of 638 recipients.
GFR Decline
There was a decline of eGFR with time in patients with PTA. There was a difference of 5.26 mL/min/1.73 m2 in eGFR between
6 months & 2 years.
Normalization of PTA to an Hb level of 13–15 g/dL reduced the rate of decline of eGFR, progression to ESRD, and improved death-censored graft survival(CAPRIT trial).
Diagnostic Evaluation
Should include:
-Red blood cell indices
-Reticulocyte counts
-Serum iron, TIBC, percent transferring saturation, & serum ferritin
-Serum folate & vitamin B12
-Tests for presence of hemolysis (haptoglobin, elevated reticulocyte counts, LDH, & indirect bilirubin).
Search for specific causes of PTA that may be unique to transplant recipients:
-Medications (IS & antimicrobial)
-Concurrent infections
-Based on evidence, a full anemia work-up 3 months post transplantation is indicated as early recognition & treatment may improve the prognosis.
Treatment of PTA
Treat the underlying cause.
No specific recommendation for the treatment of kidney transplant recipients.
Anemia (Hb < 12.5 g/dL) was significantly associated with mortality in patients with & without ESA (study of 1,794 recipients in Austria, between 1992 &2004).
In patients without ESA, a spontaneous rise in Hb was associated with decreased mortality at any level.
In patients treated with ESA, improvement of anemia (Hb up to 12.5 g/dL) was associated with decreased mortality as well.
Further increments in Hb levels led to a tendency toward increased rates of mortality, which became significant at
Hb levels > 14 g/dL.
Normalization of PTA (Hb levels of 13–15 g/dL) with epoetin-β reduced the rate
of decline of the estimated creatinine clearance, the eGFR, & progression to ESRD & improved death-censored graft survival.
Quality of life also improved with full correction.
There were no cardiac disorders (HF, arrhythmia, or MI) in the full-correction group.
Both the CHOIR trial & the TREAT reported an increased risk of CV events & no delay in progressive renal failure by targeting normalization of Hb with ESA therapy.
CREATE trial showed that randomization to a higher Hb target significantly increased the likelihood of initiation of chronic dialysis.
KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL.
The NKFKDOQI guidelines endorsed the FDA-recommended upper cut-off of 11 g/
dL. No specific recommendation was made
for transplant recipients.
The CAPRIT trial in transplanted is the only RCT addressing this question in the transplanted population. The results suggest that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD & should probably be up to 12–13 g/dL.
A larger RCT, designed like the CAPRIT
study, with a longer follow-up may help to define the target Hb level.
Studies of treatment with iron in transplant recipients are scarce.
A small RCT (104 patients) comparing oral versus a single dose of IV iron after transplantation did not show a difference in time to anemia correction above 11 g/dL.
A meta-analysis showed the safety of IV iron for all indications; so it seems reasonable to treat transplanted patients
with IV iron. ================ What is the level of evidence provided by this article? Level V ================ What is meant by the impact factor of a journal (please in your own words)?
Impact factor of a journal is a method by which to assess the importance of that journal. The higher is the impact factor of a journal, the more it is cited to different articles (books, thesis, journals etc); it has nothing to do with the quality of the contents of that journal. Also the journal should have completed at last 3 years from its first publication to be eligible for being assessed by impact factor.
Dear All
How is the impact factor calculated?
What is the bias involved in relying on the impact factor to assess journals?
The impact factor is calculated by dividing the number of citations in the JCR year by the total number of articles published in the two previous years
The impact factor is just a measure of the number of citations a journal gets over a time period. It is not based on any peer review. The article from the journal can be cited in non-peer review journals, books, thesis, presentations. New journals, because of the time period of two years, don’t have an impact factor and may be considered not to be very relevant in that particular field
The Impact Factor is calculated by dividing the number of citations in the journal citation report per year by the total number of articles published in the two previous years.
The ratio of number of citations in a particular journal over the previous two years to the number of publications in the journal over the same period of time
-Some journals may not have a high impact factor which may lead to their underestimation and yet the are still a good journals
The journal Impact Factor is the average number of times articles from the journal published in the past two years have been cited in the Journal citation report year. The Impact Factor is calculated by dividing the number of citations in the Journal citation report year by the total number of articles published in the two previous years. Journals may be biased toward positive results because negative results are less likely to be cited and can thus lower a journal’s impact factor
Impact factor of a journal = Total number of times its articales were cited during the two previous years ÷ Total number of citable articales in the journal during those two years.
How is Impact Factor(IF) calculated?
Calculation is based on a two-year period and involves number of times articles were cited divided by the number of citable articles.
For Example: Calculation of 2021 IF of journal
A=the number of times articles [published in 2019 and 2020] were cited by indexed journals during 2021
B=Total number of citable articles published by journal in 2019 and 2020
A/B=2021 IF of journal
It is used to evaluate the importance or rank of a journal by calculating the times its articles are cited.
What is the bias involved in relying on the impact factor(IF) to assess journals?
Self-Citation Bias: If self-citations are used in the introduction or discussion, to stress one’s own conviction, this could lead to bias.
The probability of being cited seems more associated with positive study outcomes (supportive Publications), the authority of its authors and the journal in which it is published.
Reviews would have a higher probability of being cited than original Research studies. Also, original research studies will be less cited once they have been taken up in a (systematic) review.
Journals publishing many review articles usually have high Impact Factors, because review articles usually have a higher average rate of citation than empirical studies/original papers.
Higher sample size study is likely to be more cited than small sample size irrespective of quality of study design.
Journals with large number of articles published are more likely to contain highly cited articles and high IF than journals with small numbers of articles published.
Quality of study is not correlated with citation. citation does not reflect the scientific merit of the cited work and articles are cited for various reasons
Two years duration is less for assessing how important is the journal. Articles cited within two years after publication contribute to the impact factor although many landmark papers achieve their maximal scientific impact outside of this timeframe.
Differences in citation patterns among disciplines are not considered, which makes it impossible to compare journals across disciplines.
the impact factor of a journal is calculated by dividing the number of current year citations to the source items published in that journal during the previous two years.
Limitations and bias:
the impact factor is calculated by dividing the number of citations in the journal citation report per year by the total number of articles published in the two last years.
IF is calculated as the number of one year citations in a journal divided by the number of articles published in that journal during the last two years.
Dear professor ,
The impact factor is calculated by dividing the number of citations in the journal citation report per year by the total number of articles published in the past-previous 2 years.
A two year time period may over or underestimate the strength of the journal .
Posttransplantation anemia ( PTA ) is common among kidney transplant recipients.
Early PTA is defined as anemia which develops up to 6 months after transplantation and is the predictor for late PTA
Late PTA is defined as anemia which develops after 6 months and associated with impaired graft function
Iron deficiency being the major contributor for IDA.
PTA is associated with increase mortality, reduced graft survival, and a decline in GFR.
Treatment of PTA should probably begin as soon as possible with ESA and IV Iron. The optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL.
Level 5 evidence.
Impact factor is a scientometric index that reflects the yearly mean number of citations of a journal in the last two years.
Post transplant anemia PTA is a common problem,prevalence range from 20-50%
the main cause is iron deficiency
the target Hb should be more than 13g/dl
full panel investigation of serum iron,TIBC,B12 ,folate ,retics count,bilirubin and lactate dehydrogenase
treatment with replacement of the deficit and erythropoietin stimulating agent.
Level 5 evidence
post transplantation anemia is a common health problem that affect up to 50 % of kidney recipients and defined as HB <12g/dl in females and <13 g/dl in males. Post transplantation anemia has negative impact on graft survival, GFR and recipient mortality specially in severe anemia.
Post transplantation anemia is classified into early (during 1st 6 month after transplantation) and late (after more than 6 months from transplantation).
Causes of post transplantation anemia
1- Early onset: mainly due to iron deficiency, poor nutrition, perioperative blood loss and increase erythropoietin production from the graft stimulating erythropoiesis.
2- Late onset anemia:
iron deficiency, myelosuppressive effect of IS drugs, infection, inflammation and decrease graft function
Risk factors for post transplantation anemia
1- Early onset anemia is related to female sex, hypochromic RBCs before transplantation and low e GFR.
2- Late onset anemia: early onset anemia is a risk factor for late onset anemia, female patient, donor age, S Cr
Nutritional deficiency including B12 and folic acid
Diagnosis of post transplantation anemia
Same approach as non-transplant patients
1- CBC, iron profile, vit B12 and folic acid levels, reticulocytes, comb test, LDH
Treatment
No specific KDIGO recommendations for treatment of post transplantation anemia but most studies recommend correct to HB level 13-15 g/dl through replacement of iron, B12 and folic acid in case of their deficiency and consider erythropoietin therapy to reach target HB.
-Level of evidence is V
-Impact factor is used to express the scientific importance of a journal through measuring the frequency of citation of this journal articles during certain time period.
Post transplant anemia PTA
Prevelance 20 to 51%
Early PTA is anemia which develops up to 6 months after transplantation.
Late PTA is anemia which develops after 6 months.
Anemia is defined as hemoglobin levels< 12g/ dl in women and < 13 g/dl in men.
Causes and predictive factors for PTA
Early PTA occurs due to iron deficiency which occurs secondary to depletion of iron stores before transplant, perioerative blood loss and poor nutrition or may be secondary to increased iron utilization with onset of erythropoiesis.
Late PTA due to reduced graft function and development of renal insufficiency, iron deficiency, inflammation, infection , Immunosuppressive drugs ( MMF and Azathioprine) and medications affecting the renin angiotensin aldosterone systems( ACEi , ARBs ) , Trimethoprim sulfamethoxazole and Ganciclovir.
Outcomes of patients with PTA
PTA is associated with reduced mortality, reduced graft survival and decline of GFR.
Anemia was independent risk factor for LVH 1 to 5 years after transplantation. LVH and anemia were associated with a significant risk of death.
Diagnosis
Assessed for usual causes of anemia in non transplant patients
RBC indicies , reticulocyte count , serum iron , transferrin, transferrin saturation, serum ferritin , folate , vitamin B12, haptoglobulin and LDH.
Full anemia work up 3 months post transplant vfor Early detection and early management
Management.
The optimal target hemoglobin level in kidney transplantation is higher the target in haemodialysis and should be up tom12.5 to 13 gm/dl.
With using erythropoiesis – stimulating agents ( ESA ) and iron if indicated.
Impact factor is the average number of citations per year to the recent articles published in that journal.
Anemia is defined by WHO as hemoglobin levels < 12 g/dL in women and < 13 g/dL in men. It can occur early (up to 6 months after transplantation) with 50% prevalence and late (after 6 months) with 23–35% prevalence.
Causes of and Predictive Factors for post-transplant anemia (PTA)
Early PTA causes are is usually due to iron deficiency due to depletion of iron stores before transplantation, perioperative blood loss, poor nutrition and increased iron utilization with the onset of erythropoiesis.
Late PTA is associated with impaired graft function , iron deficiency, inflammation and infection, immunosuppressive medications, RAS I, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir
factors associated with early PTA included: female sex, lower eGFR , and hypochromic red blood cells.
Factors significantly associated with late PTA included early PTA, graft function; donor age, the use RAS I , the use of immunosuppressive drugs such as mycophenolate mofetil and azathioprine, a recent infection, 3-month creatinine levels and female sex
Outcomes of Patients with PTA
Mortality and Graft Failure
Cardiovascular Morbidity, left ventricular hypertrophy and de novo congestive heart failure
GFR Decline
Diagnostic Evaluation
1- red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12,
2- tests for presence of hemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin).
3- specific causes of anemia such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc
4- a full anemia work-up approximately 3 months post transplantation for early recognition
Treatment of PTA
The management of PTA starts with diagnosis and treatment of all reversible causes .Hb target is 12.5 – 14 g/dL
KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL [40]. The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative and targeting (NKFKDOQI) guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/ dL [45]. Again, no specific recommendation was made for transplant recipients.
The CAPRIT trial in transplanted patients suggest that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL.
level of evidence is 5
Impact factor is used to evaluate the relative journal importance and to measure the frequency of citation of its average article in a particular time period.
Posttransplantation Anemia in Kidney Transplant Recipients
Prevalence and Epidemiology:
PTA is widespread, with an incidence ranging from 20-51% depending on the time post-transplant.
Hemoglobin (Hb) levels below 12 g/dL for women and 13 g/dL for males are considered anemic by the World Health Organization (WHO) and the American Society of Transplantation, respectively.
Up until 8 years following transplantation, the frequency of late PTA reduces to about 23-35% at various times.
Causes of and Predictive Factors for PTA:
The typical definition of early PTA is anemia that appears up to six months following transplantation.
It is primarily brought on by a lack of iron.
Anemia that manifests after six months is referred to as late PTA. and it might not show up for up to 8 years.
Late PTA has been linked to diminished graft function and the emergence of renal insufficiency.
Other factors that may contribute to anemia include iron deficiency, infection, immunosuppressive drugs like mycophenolate mofetil, mycofenolic acid, and azathioprione, drugs that affect the renin-angiotensin-aldosterone system like angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobials like trimethoprim-sulfamethoxazole, and antivir
Predictors of PTA:
female sex ,lower eGFR ,hypochromic red blood cells
Early PTA and the use of a living donor as the source of the transplant were both protective factors that were also strongly associated with late PTA (2 years after the transplant).
age of the donor (especially if over 60), use of ACE inhibitors or angiotensin receptor blockers, recent infection, and use of immunosuppressive medications such mycophenolate mofetil and azathioprine.
Etiology of PTA:
The most frequent contributing cause to early PTA is iron insufficiency.
Iron insufficiency can arise for a variety of reasons, including inadequate iron storage at the time of transplantation, blood loss during surgery, increased iron usage with the onset of erythropoiesis, and inadequate diet.
In various investigations, vitamin B12 deficiency was identified as the root cause of PTA in 17–24% of individuals.
10% of the cases in our study were caused by folic acid deficiency, which is a comparatively low percentage compared to the 23-41% described in previous studies.
Acute renal injury, which accounted for 11.4% of instances of PTA, and acute rejection, which accounted for 4% of cases. In 19% of cases, infections were the root cause of anemia.
Outcomes of Patients with PTA:
PTA is linked to decreased GFR, decreased graft survival, and lower death.
The severity of the anemia and its specific causes are linked to the connection with mortality.
Diagnostic Evaluation :
Red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12, as well as tests for the presence of hemolysis (haptoglobin) when clinically indicated, are used to evaluate the usual causes of anemia in non-transplanted patients (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin). Additionally, it is important to look for any specific probable reasons of anemia that may be unique to people who have had a kidney transplant, such as the use of immunosuppressive and antimicrobial medicines, concurrent infections, etc.
Treatment of PTA:
All reversible causes should be diagnosed and treated.
Several issues should be addressed:
Target Hb level for treatment
Type of treatment
anemia (Hb <12.5 g/dL) was significantly associated with mortality in patients with and without ESA. In patients without ESA.
A spontaneous increase in Hb was linked to lower mortality at any level in individuals without ESA. Improvement in anemia (Hb up to 12.5 g/dL) in individuals using ESA was also linked to a lower mortality rate.
As with CKD patients, if ESA is started, the iron status should be determined and the iron stores should be filled.
Whether intravenous iron is superior to orally taken iron in the context of transplantation is a matter of debate.
As soon as possible following a kidney transplant, PTA treatment should start.
The ideal goal Hb level for kidney transplant recipients with anemia should likely be between 12.5 and 13 g/dL, which is higher than the target advised for CKD. It is necessary to have appropriate treatment with ESA and intravenous iron in order to meet this goal.
Level 5
Imapct factor can be calculated by the number of citations received by the article in one year divided by total number of cited articles in the same journal.
Introductions:
Posttransplant anemia is common problem, associated with increase mortality and graft dysfunction.
Prevalence:
Between 21 -50perecdnt.hemoglobin less than 13 in male and 12 mg/dl is define anemia.
Early posttransplant anemia occur before 6 months and late after 6 months .
Etiology. And risk factor:
Most common. Due to iron deficiency either pre transplant or due to blood loss during operation or nutritional deficiency .also increased utilization of iron postarnsplant can predispose to iron deficiency.
Vitamins B deficiency and folic acid deficiency. Is less common cause.
Other cause of anemia as infection and drugs should ask be considered.
Risk Factors :
Female gender and early posttransplant anemia is known risk factors in addition to glomerular filtration rate.
Complication of PTA:
Increased morality.
Heart failure.
Left ventricular hypertrophy.
Reduce graft function .
Diagnoses:
Baseline hematological indices
Hemoglobin MCV MCHC,iron study ,ferritin, Saturation
In addition to reticulocyte count ,haptoglobin .
Serum vitamin b and folic acid.
Treatment:
Treatment. Of underlying cause.
Iron and ESA to keep hemoglobin level between 12 _13gram.
Level of evidence 5.
Impact factor is total number of citation over last two years divided by number of articles
published in the journal .
Introduction
Anemia · Kidney transplant · Posttransplantation anemia Abstract
Posttransplantation anemia (PTA) is common among kidney transplant patients. Early PTA is usually defined as anemia which develops up to 6 months after transplantation, and late PTA is defined as anemia which develops after 6 months. There are multiple causes, with iron deficiency being the major contributor. The occurrence of late PTA has been associated with impaired graft function. Early PTA has been shown to be a predictor of late PTA. PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anemia and to specific causes of anemia. Treatment of PTA should probably begin as soon as possible after kidney transplantation. The optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with erythropoiesis-stimulating agents (ESA) and iron is indicated.
Causes of and Predictive Factors for PTA
Early PTA is usually due to iron deficiency. Iron deficiency may be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition. In addition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia
Late PTA is usually defined as anemia that occurs
more than 6 months after transplantation, and it can appear as late as up to 8 years later . The occurrence of late PTA has been associated with impaired graft function and the development of renal insufficiency .Late PTA is predominantly influenced by a reduced allograft function.
Predictors of PTA
Several studies have aimed to find predictors of PTA. In a retrospective study by our group . 266 patients who underwent kidney transplantation at the Rabin Medical Center in Israel, a single tertiary center, during a 4-year period (2008–2011) were included .
Etiology of PTA Iron deficiency is the most common contributing factor for early PTA. Inadequate iron stores at the time of transplantation, blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition all contribute to the occurrence of iron deficiency
Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies . Folic acid deficiency was the cause of anemia in 10%
of the cases in the study by our group [2], which is a relatively low rate compared to the 23–41% reported in other studies .Other causes of PTA in our cohort included acute kidney injury, accounting for 11.4% of cases, and acute rejection, accounting for 4% of cases. Infections were the cause of anemia in 19% of cases
Outcomes of Patients with PTA Mortality and Graft Failure
PTA has previously been shown to be associated with the composite outcome of all-cause mortality and graft loss. However, while almost all of the studies have shown a significant correlation with graft failure, results regarding the association between anemia and mortality are inconsistent.
Cardiovascular Morbidity
A retrospective Canadian cohort study conducted in 473 renal transplant recipients showed that anemia and was an independent risk factor for left ventricular hypertrophy (according to Cornell electrocardiographic voltage criteria) 1–5 years after transplantation
GFR Decline In the retrospective study by our group, there was a
decline of eGFR with time in patients with anemia. There was a difference of 5.26 mL/min/1.73 m2 in eGFR between 6 months and 2 years. The eGFR in anemic patients declined by 2.26 mL/min/1.73 m2 while the eGFR increased in nonanemic patients
Diagnostic Evaluation
The diagnostic evaluation of renal transplant recipients should include an assessment for “the usual” causes of anemia as with nontransplanted patients, i.e., red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin). In addition, specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc., should be sought. Based on published evidence, a full anemia work-up approximately 3 months post transplantation is indicated as early recognition and treatment may improve the prognosis.
Treatment of PTA
The management of PTA starts with diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause. However, there is no specific recommendation for the treatment of kidney transplant recipients
Several issues regarding specific treatment should be addressed. Most importantly, the target Hb level for treatment, followed by the type of treatment, i.e., erythropoiesis-stimulating agents (ESA) and/or iron, should be determined.
The results of the CAPRIT trial are different from
those observed in larger trials in the CKD population. The Correction of Hemoglobin and Outcomes in Renal Insufficiency (CHOIR) trial included 1,432 CKD stage 3–4 patients who were randomized to achieve a target Hb level of 13.5 or 11.3 g/dL using epoetin-α. The Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT) included 4,038 patients with type 2 diabetes and CKD stage 3–4 to achieve a target Hb. Patients were randomized to either darbepoetin-α to achieve an Hb target of 13.0 g/dL or placebo with rescue darbepoetin-α when the Hb concentration was < 9.0 g/dL
In conclusion, PTA is a common complication of renal transplant recipients. It is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anemia. Treatment of PTA should begin as soon as possible after kidney transplantation. Based on data derived from the CAPRIT . study and the observational study by Heinze et al. [41], it appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
Level 5
Post transplantation anemia in potential kidney transplant recipients
It occurs:
Causes :
Early PTA can predict occurrence of late PTA. In late PTA, the graft function will be impaired. Whether in the early or late period, PTA can lead to reduced mortality, decreased chances of graft survival, and a reduction in GFR. The risk of mortality is linked to the severity of PTA.
Treatment is to be rapid with reaching the target hemoglobin level, up to 12.5-13 g/dL. Treatment includes ESA and iron.
Once ESA has been started, iron status is to be determined and maintained. It is not established whether IV iron or oral iron is better for transplant recipients.
Treatment should be started as soon as possible after transplant. This is essential for better outcome of transplant and to promote chances of graft survival without complications.
-Narrative review – level of evidence 5.
To calculate the impact factor, the number of citations received by the article in one year is divided by total number of cited articles in the same journal.
Summarization of the article:
An important thing is Post transplant anemia (PTA) with currency between 21-55%. Hemoglobin less than 13 in males and less than12 in females is defined as Anemia. Left ventricular failure, poor long term graft outcomes, low eGFR and Congestive cardiac failure are associated with anemia. The article discusses PTA with currency prognosis, etiology and management.
The currency rate is between 21-55% post-transplant patients.
Late PTA is anemia happening more than 6 months after the transplant, which can cause dysfunction of graft and is mostly affected by graft dysfunction. Other factors such as immune suppressants, iron deficiency, ACEi,ARBs antibiotics such as sulphathiazole and trimethoprim and antiviral might affect it.
prognosticators of late PTA can be the usage of ACEi, ARBi, living donor, infections, donor age, female sex, and low eGFR.
Early PTA is anemia happening less than 6 months after the transplant. It is caused by nutritional factors, increased iron utilization by new onset erythropoiesis after the transplantation, depleted iron stores pre transplant, and peri operative losses.
Poor graft outcome and mortality have a correlation with PTA.
Treatment of PTA includes: identification of underlying cause and its treatment, erythropoiesis stimulating agents, aiming for Hb >12.5g/dl, and Iron replacement.
The level of evidence provided by this article is Review article Level V
The tool to assess the importance of a journal is the impact factor. It is based on the number of citations to the article of this journal, during a specific period of time. Ratio of the number of citations a journal receives in the last 2 years to the number of publications of that journal in the span of the last 2 years would give us the impact factor. Cites/doc (2 years).
We can use the article from a journal as a citation in different presentations, books, and dissertation. For obvious reason, a new journal won’t have impact factor in the first 2 years which can make a bias.
Posttransplantation Anemia in Kidney Transplant Recipients
Posttransplantation anemia (PTA) is common with a prevalence of 20–51% at various time points after transplantation.
long-term outcomes of PTA:
Increase rates of all-cause mortality, graft failure, congestive heart failure, left ventricular hypertrophy and a decline in the e GFR.
PTA is not defined uniformly either in term of time or in term of the degree of anemia. However, most studies distinguish between early PTA (within 6 months) and late PTA (after 6 months).
Anemia in most studies is defined as hemoglobin (Hb) levels <12 g/dL in women and <13 g/dL in men.
Causes of and Predictive Factors for PTA
Iron deficiency may be caused by depletion of iron stores, perioperative blood loss, and poor nutrition.
The onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
B12 and folate deficiency also may contribute.
The occurrence of late PTA has been associated with impaired graft function and the development of renal insufficiency.
Medications like immunosuppression, ACEi, septrin, ganciclovir.
Predictors of PTA
Female sex, lower GFR, donor age, creatinine level, the use of ACE inhibitors or angiotensin receptor blockers, the use of immunosuppressive drugs such as mycophenolate mofetil and azathioprine, and a recent infection.
Outcomes of Patients with PTA
Mortality and graft failure
PTA has previously been shown to be associated with the composite outcome of all-cause mortality and graft loss. However, while almost all of the studies have shown a significant correlation with graft failure, results regarding the association between anemia and mortality are inconsistent.
Cardiovascular Morbidity
Anemia is an independent risk factor for left ventricular hypertrophy. LVH and anemia were associated with a significant risk of death.
GFR Decline
There was a decline of eGFR with time in patients with anemia.
Normalization of PTA to an Hb level of 13–15 g/dL reduced the rate of decline of eGFR and the estimated creatinine clearance, progression to end-stage renal disease (ESRD), and improved death-censored graft survival.
Diagnostic Evaluation
First evaluate the cause of anemia as in non-transplant recipients.
In addition, specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc., should be sought. Early treatment improve the outcome.
Treatment of PTA
The management of PTA starts with diagnosis and treatment of all reversible causes. As such, treatment
should be directed at the underlying cause. However, there is no specific recommendation for the treatment of kidney transplant recipients, erythropoietin and iron therapy are important
There is a study shows that Hgb < 12.5 g/dl was significantly associated with mortality in patients with or without ESA.
Another study shows that normalization of PTA with epoetin-B reduces the rate of decline in GFR, progression to ESRD, and improved death-censored graft survival.
the KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is <10.0 g/dL, with a target Hb level of 11.5 g/dL. However, still no specific recommendation to transplant patients.
In regard to iron therapy; iron deficiency, even without anemia, has been shown to be an independent predictor of mortality in renal transplant recipients. I.v. iron administration after transplantation increased Hb levels and reduced the eGFR decline, both of which were more pronounced in lower Hb levels.
If ESA is initiated, the iron status should be determined and iron stores should be repleted, as with CKD
patients. It is unclear in the transplant setting whether i.v. iron is better than orally administered iron.
Conclusion:
PTA is a common complication. It is associated with reduced graft survival, decrease in GFR, and mortality. The target hemoglobin in transplant recipient is higher than for CKD patients (12.5 – 13 g/dl). Treatment with iron and ESA should be started as soon as possible.
Level 5
Impact factor is calculated by dividing the number of citations of articles published by the journal in the last two years divided by the total number of articles published during the same period.
Post transplant anemia (PTA) is a common problem occurring at any time post transplant.
It is associated with increased mortality, graft failure, congestive heart failure, left ventricular hypertrophy and impaired graft function.
Prevalence and epidemiology:
PTA occurs in 20-51% of kidney transplant recipients, early PTA occurs up to 6 months after transplant and late PTA occurs after 6 months
It is defined as Hgb<12g/dl in women and <13g/dl in men.
Causes and predictive values for PTA:
Iron deficiency usually cause early PTA due to depleted iron stores pre transplant, blood loss perioperatively, poor nutrition and increased iron utilization due to increased erythropoietin produced by the graft.
Late PTA is usually due to impaired graft function, other factors include iron deficiency, inflammation, infection, some immunosuppressive agents, ACE-I and ARB, some antimicrobial and antiviral agents as ganciclovir.
Predictors of anemia:
Factors associated with early PTA were female, lower eGFR and hypochromic RBCS.
Factors associated with late PTA was early PTA
In a survey, living donor was protective andHgb was strongly associated with graft function.
Early PTA is a predictor of late PTA suggesting that the better prevention and treatment of early PTA can prevent late PTA.
Etiology:
Iron deficiency, the most common cause of early and late PTA.
In a retrospective study, nutritional deficiencies were the most cause of late PTA, iron deficiency, vitamin B12 and folic acid deficiency
Other causes were AKI, acute rejection and infections.
Outcomes of patients with PTA:
Mortality and graft failure:
PTA is significantly correlated with graft failure and mortality in several studies.
Other studies showed conflicting results regarding association between anemia and long-term mortality but anemia was significantly associated with graft loss.
Cardiovascular morbidity:
A retrospective study showed that anemia is an independent risk factor for left ventricular hypertrophy and both were associated with significant risk of death.
GFR decline:
In the CAPRIT study, normalization of PTA decreased the rate of decline of eGFR, progression to ESKD and improved death censored graft survival.
Diagnostic evaluation:
Red blood cell indices, reticulocyte count
Serum iron, TIBC, percent saturation and serum ferritin
Folate and vitamin B12
Tests for presence of hemolysis when clinically indicated
Specific cause of anemia as use of medication or concurrent infection.
It is recommended to perform anemia workup at 3 months post transplant for early recognition and treatment.
Treatment of PTA:
No specific recommendations for kidney transplant recipients
Treatment of underlying cause.
KDIGO guidelines recommend initiation of ESA in patients with CKD only when Hgb concentration<10g/dl with target Hgb 11.5
ARCT showed that optimal target Hgb in kidney transplant should be up to 12-13g/dl
Iron deficiency even without anemia was independent predictor of mortality in kidney transplant recipients.
If ESA is initiated, iron status should be determined and stores should be repleted.
A meta analysis showed that IV iron was not associated with increased risk of adverse events or serious infection so can be used in kidney transplant recipients
Level of evidence 5
Post transplantation anemia (PTA) is common complication that physicians face among post-transplant patient with a prevalence of 20–51%.
It is defined as an Hb of < 12 g/dl for women and < 13 g/dl for men post-transplant.
Long term outcomes of PTA include CHF, LVH, reduced GFR and poor graft and patient survival and increased all-cause mortality .
It can be classified as early ( first 6 months) or late ( after 6months).
Early causes include: low iron stores as a consequence of the CKD and slow increase in the level of newly graft production of erythropoietin , operative blood loss and poor nutritional status.
Late causes include: infections, inflammation, graft dysfunction, iron deficiency anemia and drugs like ACE-I & ARBS, MMF, antibiotics and antivirals.
Predictors include old donor age, living donation, female sex, low eGFR and infections.
Work-up:
– Full history to identify any sources of blood loss, history of infection and drugs
– Full blood count and iron indices(ferritin ,TSAT, Vitamin B12 and folate level).
– Blood film
– Reticulocyte count
– LDH
– Check full occult blood in stool or use Q-FIT test
– Endoscopy if required
Management:
– Aim : hemoglobin -12-13g/dl
– Treatment of the cause
– Vitamin B12 replacement for vitamin B12 deficiency and folate in case of folic acid deficiency.
– Replenish iron stores with I/V iron followed by ESAs
What is the level of evidence provided by this article?
The level of evidence: is level V (review article)
What is meant by the impact factor of a journal (please in your own words)?
The impact factor of a journal means the number of times the articles in a journal are cited over time(total number of cited articles per year divided by the number of publications in two years) time. It shows the relative importance of that journal.
Posttransplantation Anemia in Kidney Transplant Recipients.
Early PTA is defined as anemia develops up to 6 months after transplantation.
Eate PTA is defined as anemia which develops after 6 months.
There are multiple causes, with iron deficiency being the main cause . The occurrence of late PTA has been associated with impaired graft function.
Early PTA has been shown to be a predictor of late PTA.
PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR.
The optimal target hemoglobin level in kidney
transplant recipients is higher than recommended
in chronic kidney disease and should probably be up to 12.5–13 g/dL.
to achieve this target, appropriate treatment with erythropoiesis-stimulating agents (ESA) and iron is indicated.
Introduction:
Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51%.
PTA is negatively associated with
– increased rates of all cause mortality.
– graft failure .
– congestive heart failure .
– left ventricular hypertrophy.
– a decline in the estimated glomerular filtration rate (eGFR).
Prevalence and Epidemiology:
Anemia defined as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men.
The prevalence is about 50%.
Causes of and Predictive Factors for PTA:
Early PTA is usually due to iron deficiency. Late
PTA is mainly caused by a reduced allograft dysfunction.
other factors that can be acause
– iron deficiency,
– inflammation and infection,
– Medication- immunosuppressive medica tions(mycophenolate mofetil, mycofenolic acid, and azathioprione),
-Anti hypertensives drug (ACEI and ARB) antimicrobial agents such as trimethoprim-sulfamethoxazole and antiviral agents such as ganciclovir .
Etiology of PTA:
Iron deficiency is the most common cause of early PTA. In one study the prevalence of anemia was 34%, and iron deficiency anemia was 13%.
Vit- B12 deficiency was the cause of PTA in 17–24% of patients in several studies. Folic acid deficiency was the cause of anemia in 10% of the anemia cases.
Other causes may include:
– acute kidney injury 11.4%.
– acute rejection 4%.
– Infections 19%.
Outcomes of Patients with PTA:
Regarding the impact of PTA on graft loss and mortality, the result are conflicting.
Some studies shows that PTA increases graft loss and mortality while other report does not. Some study report that there is association of sever ( but not mild ) anemia with graft loss and mortality.
Cardiovascular Morbidity:
PTA is independent risk factor for left ventricular hypertrophy. Left ventricular hypertrophy and anemia were associated with a significant risk of death. Anemia was identified as an independent risk factor for de novo congestive heart failure.
GFR Decline:
Some studies report that there was a decline of eGFR with time in patients with anemia.
Other studies also suggests that anemia is associated with a decline of GFR and correction of anemia is associated with a reduction in the rate decline.
Diagnostic Evaluation:
Red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitaminB12, and tests for presence of hemolysis (haptoglobin) when clinically indicated.
And specific potential causes that is unique to renal transplant recipients, (use of medications (immunosuppressive and antimicrobial), concurrent infections.
Treatment of PTA:
treatment of all reversible causes. There is no specific recommendation for the treatment of kidney transplant recipients.
Erythropoiesis-stimulating agents (ESA) and/or iron, can be used. The target of HB 12g/dl is accepted. HG level above this is associated with increase mortality therefore it is not recommended.
Studies suggest that the optimal target Hb level in kidney transplant recipients with anemia is 12–13 g/dL.
If ESA is initiated, the iron status should be deter mined and iron stores should be repleted . It is unclear in the transplant setting whether i.v. iron is better than orally administered iron. But it is reasonable to treat transplanted patients with i.v. iron.
Conclusion:
– PTA is a common complication of renal transplant recipients.
– It is associated with reduced mortality,
-reduced graft survival, and a decline in GFR.
– The association with mortality is related to the severity of the anemia.
– Treatment of PTA should begin as soon as possible after kidney transplantation.
– It appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL.
– In order to achieve this target, ap propriate
-treatment with ESA and i.v. iron should be given.
Q2- it is review article- level of evidence is 5.
Q3-
Is the reflection of the yearly mean number of citations of articles published in the last two years in a given journal . As a journal-level metric, it is frequently used as guide for the importance of a journal within its field; journals with higher impact factor values are given the status of being more important.
Introduction:
Anaemia after transplantation is about 20-51%
Long term effects of anaemia:
· increase rate of all-cause mortality
· graft failure
· congestive heart failure
· left ventricular hypertrophy and decline in the eGFR
causes of and predictive factors for PTA:
early PTA is due to iron deficiency may be caused by depletion of iron stores before transplantation.
PTA is usually defined anaemia occurs more than 6 months after transplantation.
Late PTA caused by allograft function other than factors cause anaemia in post transplantation: infection, immunosuppression medication, medication affecting renin-angiotensin-aldosterone system, and antiviral such as ganciclovir.
Iron deficiency anaemia is the most common cause for early PTA.
B12 deficiency reported to be cause of PTA in 17-24% of patients in several studies.
Folic acid was the cause of anaemia in 10% of the cases in study group.
Other causes of PTA:
1. acute kidney injury
2. acute rejection
3. infections
Outcomes of patients with PTA:
Several studies showed that there is association with mortality.
A retrospective series 1023 transplant recipients after 3 months was associated with mortality and graft failure.
CVS mortality:
A retrospective cohort study is in depend risk factor for left ventricular hypertrophy.
GFR decline:
In retrospective study by a group there was a decline of eGFR with time in patients with anaemia.
Treatment of PTA:
Nonspecific recommendation of kidney transplant recipient.
CVS reduction early anaemia treatment Epoetin beta.
Kidigo guidelines recommended ESA when Hb<10g/dl
Target Hb in transplant 12-13 g/dl
If ESA started the non-store should repleted.
Conclusion:
PTA associated with reduced mortality, reduced graft survival, and a decline in GFR. Target Hb 12-13g/dl. Treatment with ESA and I.V iron.
the leve 5
the impact factor is measured by dividing the number of citations in the journal citation report per year by the total number of articles published in the two previous years.
Post-transplant anemia is a common event and is related to several factors, the most common being depletion of iron stores. Another very common motivation is the use of different classes of drugs that can induce some cytopenia due to myelotoxicity, or even opportunistic infections.
The value of anemia tolerated for post-transplantation is much lower than that tolerated for patients with chronic kidney disease. Anemia in most studies is defined as hemoglobin (Hb) levels < 12 mg/dl in women and < 13 mg/dl in men according to the criteria of the World Health Organization (WHO) and the American Society of Transplantation. And it is divided between early anemia (appearance up to 6 months) or late (appearance after 6 months).
And although studies have not proven an association between anemia and mortality, other outcomes such as graft failure, cardiovascular morbidity and decline in Glomerular Filtration Rate have proven association.
The diagnostic evaluation of renal transplant recipients should include an assessment for “the usual” causes of anemia as with nontransplanted patients, i.e., red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin). In addition, specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc. And the management of anemia starts with diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause. However, there is no specific recommendation for the treatment of kidney transplant recipientes.
· What is the level of evidence provided by this article?
Level 05 – narrative review
Impact factor is an attempt to measure the impact that a publication has by counting the times that its articles have been cited, establishing a rank with those that presented the highest number of citations.
Incidence of post-TX anaemia: 20-50% and is associated with increased all cause mortality, graft failure, CHF, LVH.
Causes of early(within 6 months) post TX anaemia: peri-operative blood loss, iron deficiency, increased iron consumption because of increased EPO from new renal graft.
Cause of late (more than 6 months) post TX anaemia: infection, inflammation, iron deficiency, medications (MMF, MFA, AZA, ACE.I, ARBs, TMP/SMX, ganciclovir).
Anaemia work up:
FBC, RBC Indices, Reticulocytic count, Iron profile, Folate, B12, Haptoglobin, LDH, bilirubin.
Treatment of the cause
Level II, retrospective cohort study.
Introduction
The prevalence of post transplantation anaemia is about 20–51%. Post transplantation anaemia PTA is associated with worse long-term outcomes: increased rates of all-cause mortality, graft failure, congestive heart failure, left ventricular hypertrophy, as well as decline in the estimated glomerular filtration rate (eGFR).
Prevalence and Epidemiology
Early PTA is apparent up to 6 months after transplantation while late PTA occurs after 6 months. The prevalence of early PTA is about 50%, on the other hand late PTA declines to about 23–35% at various time points up until 8 years after transplantation.
Causes of and Predictive Factors for PTA
Early PTA is mostly due to iron deficiency which is enhanced by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition along with the improvement of iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin.
The occurrence of late PTA is correlated to impaired graft function and the development of renal insufficiency. Other factors may coexist potentiating PTA as iron deficiency, inflammation, infection, immunosuppressive agents, trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir.
Predictors of PTA
Female sex, lower eGFR and hypochromic red blood corpuscles are surrogates for PTA while kidneys derived from living donations acted as a protective shield against PTA.
Early PTA is also a predictor of late PTA, so the better the prevention and treatment of early PTA the less exposure to late PTA.
Etiology of PTA
Iron deficiency is the most common contributor to late PTA according to many studies. Vitamin B12 and folic acid deficiency were reported as other less contributing causes of PTA besides infections and immunosuppressive medications.
Outcomes of Patients with PTA
Mortality and Graft Failure
Anemia was significantly associated with mortality, graft failure of average follow-up of 6 years in addition to the increased risk of death.
Cardiovascular Morbidity
Anemia and left ventricular hypertrophy as an independent risk factor for cardiovascular morbidity were studied at 1–5 years after transplantation that was associated with a significant risk of death. Anemia also was identified as an independent risk factor for de novo congestive heart failure for previously known cardiac free patients.
GFR Decline
The estimated difference of in eGFR between 6 months and 2 years in anemic patients declined by 2.26 mL/min/1.73 m2 while the eGFR improved in nonanemic patients.
Normalization of PTA to an Hb level of 13–15 g/dL reduced the rate of eGFR decline, the estimated creatinine clearance, progression to end-stage renal disease (ESRD), and improved death-censored graft survival after administration of epoetin-β.
Diagnostic Evaluation
A full anemia work-up 3 months post transplantation is indicated for early recognition and treatment aiming to improve the prognosis. Thus, treatment of PTA should begin as soon as possible after kidney transplantation. To achieve this target, proper treatment with ESA and i.v. iron should be administered.
Level of evidence is 5.
The impact factor of a journal is commonly used to evaluate the suggested relative importance of a journal within its field as well as to assess the frequency which the “average article” in a journal has been cited in a particular time period. The more the journal publishes review articles, the higher the impact factor it will achieve.
Summary:
Post transplantation anemia (PTA)
Level of evidence: Level 5
Anemia in most studies is defined as hemoglobin (Hb) levels <12 g/dL in women and <13 g/dL in men, in accordance with World Health Organization (WHO) criteria and the American Society of Transplantation
PTA is not defined uniformly either in terms of timing after transplantation or in terms of the degree of anemia. However, most authors suggest distinguishing between early PTA (up to 6 months after transplantation) and late PTA (after 6 months). The prevalence of early PTA is about 50% according to various studies and the prevalence of late PTA declines to about 23–35% at various time points up until 8 years after transplantation.
Early PTA is usually due to iron deficiency. Iron deficiency may be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition In addition, increased iron utilization with the onset of erythropoiesis. Late PTA is predominantly influenced by a reduced allograft function. However, other factors, i.e., iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia .
Outcomes of Patients with PTA:
Mortality and Graft Failure : PTA has previously been shown to be associated with
the composite outcome of all-cause mortality and graft
loss. However, while almost all of the studies have shown
a significant correlation with graft failure, results regarding the association between anemia and mortality are inconsistent. Several studies have documented an association with
mortality. A retrospective multicenter analysis using a French database that included 4,217 transplant recipients showed that PTA at 12 months was associated with mortality and graft failure . A prospective cohort study of 938 kidney transplant recipients in Hungary showed PTA
to be associated with mortality and graft failure at the 4-year follow-up . in a large
retrospective analysis of 2,031 transplant recipients in Austria, anemia was significantly associated with mortality and graft failure at a median follow-up of 6 years
Cardiovascular Morbidity: A retrospective Canadian cohort study conducted in 473 renal transplant recipients showed that anemia andwas an independent risk factor for left ventricular hypertrophy (according to Cornell electrocardiographic voltage criteria) 1–5 years after transplantation. Left ventricular hypertrophy and anemia were associated with a significant risk of death. Another retrospective cohort study conducted in 2 Canadian centers included 638 consecutive adult renal transplant recipients who were free of cardiac disease 1 year after transplantation. Anemia was identified as an independent risk factor for de novo congestive heart failure
GFR Decline: In the retrospective study by our group, there was a
decline of eGFR with time in patients with anemia. There was a difference of 5.26 mL/min/1.73 m2 in eGFR between 6 months and 2 years. The eGFR in anemic patients
declined by 2.26 mL/min/1.73 m2 while the eGFR increased in nonanemic patients [1]. In the prospective randomized CAPRIT (Correction of Anemia and Progression of Renal Insufficiency in Transplant Patients) trial , patients were randomized to receiving epoetin-β with a target of 13–15 or 10.5–11.5 g/dL. Normalization of PTA to an Hb level of 13–15 g/dL reduced the rate of decline of eGFR and the estimated creatinine clearance,
progression to end-stage renal disease (ESRD), and improved death-censored graft survival. This suggests that anemia is associated with a decline of GFR and correction
of anemia is associated with a reduction in the rate decline.
Level 5 * review
Impact factor is used to evaluate relative importance of the journal in the field
Briefly summarise this article
-Posttransplantation anemia (PTA) prevalence is 20–51% at various time points after transplantation .
-PTA has been shown to be negatively associated with the following long-term outcomes: increased rates of all-cause mortality , graft failure , congestive
heart failure , left ventricular hypertrophy , and a decline in the estimated glomerular filtration rate (eGFR) .
-Early PTA (up to 6 months after transplantation) and late PTA (after 6 months) .
-Early PTA is usually due to iron deficiency (Inadequate iron stores at the time of
transplantation, blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition all contribute to the occurrence of iron deficiency).
-The occurrence of late PTA has been associated with impaired graft function
and the development of renal insufficiency .
-Late PTA is predominantly due to a reduced allograft Function , iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin- aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir.
-Factors associated with early PTA included: female sex , lower eGFR , and hypochromic red blood cells.
– Factors significantly associated with late PTA (2 years after transplantation) included early PTA, and a living donor as the transplantation source was protective .
-Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies and folic acid deficiency was the cause of anemia in 10% of the cases.
– PTA at 12 months was associated with mortality and graft failure .
– Both severe and mild anemia were associated with graft failure.
-Left ven tricular hypertrophy and anemia were associated with a significant risk of death and anemia was an independent risk factor for de novo congestive heart failure .
– Anemia is associated with a decline of GFR and correction of anemia is associated with a reduction in the rate decline.
-The diagnostic evaluation of renal transplant recipients should include an assessment for red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when
clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin).
-The management of PTA starts with diagnosis and treatment of all reversible causes. However, there is no specific recommendation for the treatment of
kidney transplant recipient.
-Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD and improved death-censored graft survival.
-Both the CHOIR trial and the TREAT demonstrated an increased risk of
cardiovascular events and no delay in progressive renal failure by targeting normalization of Hb with ESA therapy.
-Based on these studies the KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL .
-The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative and targeting (NKFKDOQI) guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/ dL .
-No specific recommendation was made for transplant recipients.
-The CAPRIT trial in transplanted patients suggest that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL.
-Iron deficiency, even without anemia, has been shown to be an independent
predictor of mortality in renal transplant recipients .
-It is retrospective cohort study that included 81 patients who received intravenous (i.v.) iron after transplantation between 2000–2009; i.v. iron
administration after transplantation increased Hb levels and reduced the eGFR decline, both of which were more pronounced in lower Hb levels.
What is the level of evidence provided by this article?
Level 5
What is meant by the impact factor of a journal (please in your own words)?
In any given year, the two-year journal impact factor is the ratio between the number of citations received in that year for publications in that journal that were published in the two preceding years and the total number of “citable items” published in that journal during the two preceding years.
Summary – Posttransplantation anemia in kidney transplant recipients
This article revolves around post transplant anemia developing in kidney transplant recipients. This can be found in different time frames following the transplant.
Causes :
Early PTA can predict development of late PTA. If late PTA occurs, it is possible that graft function will be impaired. Whether in the early or late period, any kind of PTA can lead to reduced mortality, decreased chances of graft survival, and a reduction in GFR. The risk of mortality in each of these patients is linked to the severity of PTA.
Treatment is to be prompt with restoration of target hemoglobin level, up to 12.5-13 g/dL. Treatment options include ESA or erythropoietin stimulating agents and iron.
Once ESA has been started, iron status is to be determined and repleted. It is not confirmed whether IV iron or oral iron is better for transplant recipients.
Treatment should be started soon after transplant without delay. This is essential for good outcome of transplant and to boost chances of graft survival without unnecessary complications.
Level of evidence
Narrative review – level of evidence 5.
Impact Factor
Impact factor is the average number of times a given article has been cited within the JCR year. To calculate the impact factor of an article, the number of citations received by the article in one year is divided by total number of cited articles in that journal.
Post-transplant anemia (PTA) is common clinical problem among kidney-transplant patients with prevalence 20 – 51 % at various time points.
According to WHO criteria and the American Society of Transplantation, anemia is defined as hemoglobin (Hb) levels below < 12 g/dl in women and < 13 g/dl in men.
Classification :
1- Early PTA : occur up to 6 months after transplantation
2- Late PTA : occur after 6 month
Causes of PTA:
Early PTA can be caused by :
1- iron deficiency
2- operation associated bleeding
3- poor nutrition
4- low erythropoietin secretion of the new graft.
Late PTA causes include:
1- Impaired graft function and renal failure
2- Iron deficiency, vitamin B12 and folic acid deficiencies.
3- Infection and inflammation
4- Immunosuppressive drugs like (mycophenolate mofetil, mycofenolic acid, and azathioprione),
5- Medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting
enzyme inhibitors and angiotensin receptor blocker
6- Antimicrobial agents such as trimethoprim-sulfamethoxazole,
7- Antiviral agents such as ganciclovir.
Complications of PTA:
1- Increased mortality and graft loss
2- Cardiovascular morbidity
3- Decline of GFR
Diagnosis of PTA:
1- CBC and red blood indices
2- Reticulocyte count
3- serum iron, total iron-binding capacity (transferrin), transferrin saturation, serum ferritin
4- Folate level and vitamin B12
5- Hemolysis indicators like haptoglobin, elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin.
Treatment of PTA :
Should be directed according to the underlying cause.
There is no specific recommendation for the treatment unlike the situation in chronic kidney disease.
Anemia in most studies is defined as hemoglobin (Hb) levels <12 g/dL in women and <13 g/dL in men, in accordance with World Health Organization (WHO) criteria and the American Society of Transplantation.
Post-transplant anemia can be divided into Early PTA (up to 6 months after transplantation) and late PTA (after 6 months)
Causes of and Predictive Factors for PTA
Early PTA is usually due to iron deficiency which can be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition. In addition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
Late PTA is usually defined as anemia that occurs more than 6 months after transplantation, and it can appear as late as up to 8 years later. The occurrence of late PTA has been associated with impaired graft function and the development of renal insufficiency.
However, other factors, i.e., iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia
Treatment of PTA
The management of PTA starts with diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause. However, there is no specific recommendation for the treatment of kidney transplant recipients
The impact factor (IF) is a measure of the frequency with which the average article in a journal has been cited in a particular year
The impact of a journal in a particular year =
The total number of its articles were cited within previous 2 years
—————————————————————————————- ÷
The total number of citable articles in the journal during same those 2 years
Posttransplantation anaemia( PTA) is common among kidney-transplant patients, with a prevalence of 20–51%.
It is negatively associated with the following long-term outcomes: increased all-cause mortality rates, graft failure, congestive heart failure, left ventricular hypertrophy, and a decline in the eGFR.
Prevalence and Epidemiology
up to 20–51% of patients remain anemic after transplantation at various times post-transplant.
most authors suggest distinguishing between early PTA (up to 6 months after transplantation) and late PTA (after 6 months).
The prevalence of early PTA is about 50% according to various studies and the prevalence of late PTA declines to about 23–35% at various time points up until 8 years after transplantation.
Causes of and Predictive Factors for PTA :
Predictors of PTA:
In multivariate analysis, factors associated with early PTA:
factors associated with late PTA:
Etiology of PTA:
Outcomes of Patients with PTA:
Mortality and Graft Failure:
Almost all of the studies have shown a significant correlation with graft failure, and results regarding the association between anaemia and mortality are inconsistent.
Cardiovascular Morbidity:
anaemia showed to be an independent risk factor for left ventricular hypertrophy in a retrospective study. Also, it was identified as an independent risk factor for de novo congestive heart failure in another study.
GFR Decline:
In a retrospective study, The eGFR in anemic patients declined by 2.26 mL/min/1.73 m2 while the eGFR increased in nonanemic patients.
Diagnostic Evaluation:
Treatment of PTA:
no specific recommendation for the treatment of kidney transplant recipients.
the target Hb level for treatment, type of treatment, i.e., erythropoiesis-stimulating agents (ESA) and/or iron, should be determine.
treatment should be directed at the underlying cause.
Based on data derived from the CAPRIT study and the observational study, it appears that the optimal target Hb level in kidney transplant recipients with anaemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL.
In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
Level 5 (review article)
Impact factor is commonly used to evaluate the relative importance of a journal within its field and to measure the frequency with which the “average article” in a journal has been cited in a particular time period.
Briefly summarise this article
Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation
PTA associated with
· increased rates of all cause mortality
· graft failure
· congestive heart failure
· left ventricular hypertrophy
· decline in eGFR
There are early PTA (up to 6 months after transplantation) and late PTA (after 6 months)
Definition of anemia: hemoglobin (Hb) levels <12 g/dL in women and <13 g/dL in men
Early PTA is occurring in 50% while late PTA declines to about 23–35% at various time points up until 8 years after transplantation
Causes of and Predictive Factors for PTA
Early PTA is usually due to iron deficiency which could be due to:
· depletion of iron stores before transplantation
· perioperative blood loss
· poor nutrition
· increased iron utilization with the onset of erythropoiesis with slowly increasing
levels of the newly graft-produced erythropoietin
late PTA has been associated with
· impaired graft function and the development of renal insufficiency
· iron deficiency
· inflammation and infection
· immunosuppressive drugs (MMF, MFA, and azathioprione)
· angiotensin-converting enzyme inhibitors and angiotensin receptor blockers
· antimicrobial agents such as trimethoprim-sulfamethoxazole
· antiviral agents such as ganciclovir
Predictors of PTA
Risk factors for early PTA: female sex, lower eGFR, and hypochromic red blood cells
Risk factors for late PTA: early PTA, Graft dysfunction, Donor age (mainly > 60 y), and female gender
Etiology of PTA
· Iron deficiency is the most common contributing factor for early PTA mostly due to: Inadequate iron stores at the time of transplantation, blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition
· Vitamin B12 deficiency is the cause of PTA in 17–24% of patients
· Folic acid deficiency was the cause of anemia in 10% of the cases
· acute kidney injury in 11.4% of cases
· acute rejection in 4% of cases
· Infections were the cause of anemia in 19% of cases
Outcomes of Patients with PTA
· Severe anemia (Hb <11 g/dL)was associated with mortality while mild anemia was not
· Both severe and mild anemia were associated with graft failure
· anemia an independent risk factor for left ventricular hypertrophy 1–5 years after transplantation
· Left ventricular hypertrophy and anemia were associated with a significant risk of death
· there was a decline of eGFR with time in patients with anemia
Diagnostic Evaluation
red blood cell indices, reticulocyte counts, serum iron, TIBC (transferrin), serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when clinically indicated (elevated reticulocyte counts, lactate dehydrogenase, and indirect bilirubin.
Drug or infection history
Treatment of PTA
· diagnosis and treatment of all reversible causes
· erythropoiesis-stimulating agents (ESA) and/or iron as CKD guidelines
· If ESA is initiated, the iron status should be determined and iron stores should be
repleted, as with CKD patients
· optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL
What is the level of evidence provided by this article?
Cohort study. Evidence level 2
What is meant by the impact factor of a journal (please in your own words)?
It is a calculation indicates the importance of a Journal to its field. IF cannot be calculated for new journals, only after completing of 3 years of publication.
The IF of any journal may be calculated by the formula (e.g., in 2012)
2012 impact factor =A/B
Where A is the number of times articles published in 2010 and 2011 were cited by indexed journals during 2012. B is the total number of citable items like articles and reviews published by that journal in 2010 and 2011
What is the bias involved in relying on the impact factor to assess journals?
IF evaluation is based on a sample that may represent half the whole-of-life citations to some journals, but a small fraction (<10%) of the citations accruing to other journals. This disproportionate sampling means that the IF provides a misleading indication of the true impact of journals, biased in favour of journals that have a rapid rather than a prolonged impact.
Post-transplantation Anemia in Kidney Transplant Recipients(PTA)
– Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51%
– can be divided into:
· Early PTA: developed within 6 months post-transplant .
· Late PTA: developed after 6 months post-transplant .
– The optimal target Hb level in KTR >>12.5 to 13 g/dl.
Causes :
– Iron deficiency as a result of depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition, increased iron utilization.
– chronic allograft injury , iron deficiency, inflammation, infection, immunosuppressive medications, antiviral agents (ganciclovir), TMP/SMX, ACEI and ARBs.
Predictors :
– Early PTA: female sex and low GFR.
– Late PTA: early PTA , female sex , 3-months creatinine level (SCr >2mg/dl), donor age >60, infection and drugs ( use of MMF, AZA, ACEI, TMP/SMX).
Outcome :
– all cause Mortality and graft failure increased with Hb <11g/dl.
– Cardiovascular morbidity( anaemia is an independent risk factor for LVH).
– Decline of GFR (The eGFR in anemic patients declined by 2.26 mL/min/1.73 m2 while the eGFR increased in nonanemic patient).
Diagnostic evaluation:
– usual work up : RBCs indices, retics count, iron study, folate and vit B12 level.
– search for Haemolysis: haptoglobin level, retics count, bilirubin and LDH.
– Potential causes of anaemia should be sought( drugs, infection).
Management :
– Diagnosis and treatment of all reversible causes.
– target>> hb.>>12-13.5
– Iron oral or IV &
– erythropoietin stimulating agents
>>>>>Level of evidence >>level 5.
The Impact factor (IF) is an index that reflects the yearly mean number of citations of articles published in the last two years in a given journal
Calculation:
– In any given year, the two-year journal impact factor is the ratio between the number of citations received in that year for publications in that journal that were published in the two preceding years and the total number of “citable items” published in that journal during the two preceding years
– For example :
IF (2020) = citations in 2020 / (publications in 2019 + publications in 2018 )
Posttransplantation anemia (PTA) is common among KTRs, with a prevalence of 20–51%
It has been shown to be negatively associated with:
1. Increased rates of all cause mortality
2. Graft failure
3. Congestive heart failure
4. LVH
5. Decline in eGFR
Prevalence and Epidemiology
KT may correct anaemia, but up to 20–51% of patients remain anaemic after transplantation
Two main types:
1. Early PTA (up to 6 months after transplantation)- 50% of cases
2. Late PTA (after 6 months) occurs in 23-35%
Causes of and Predictive Factors for PTA
1-Early PTA is usually due to IDA
2-Late PTA -associated with impaired graft function and the development of renal insufficiency. Late PTA is predominantly influenced by a reduced allograft function.
other factors:
iron deficiency
inflammation and infection
IS- Mycophenolate mofetil, mycofenolic acid, and azathioprione
medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers
antimicrobial – as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anaemia
Predictors of PTA
· Female sex.
· Lower eGFR.
· Hypochromic red blood cells
Factors significantly associated with late PTA (2 years after transplantation) included:
· Early PTA, (HR 0.601; 95% CI 0.453–0.799, for every
· Living donor as the transplantation source was protective
· Donor age above 60 years
· Use of ACE inhibitors or angiotensin receptor blockers
· Use of IS – mycophenolate mofetil and azathioprine.
· Recent infection
Aetiology of PTA
· IDA – common contributing factor for early PTA.
Due to:
1. Inadequate iron stores at the time of transplantation.
2. Blood loss during surgery.
3. Increased iron utilization with the onset of erythropoiesis.
4. Poor nutrition
· Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies.
· Folic acid deficiency was the cause of anaemia in 23-41%
· Acute kidney injury, accounting for 11.4% of cases, and
· Acute rejection, accounting for 4% of cases.
· Infections were the cause of anaemia in 19% of cases.
Outcomes of Patients with PTA
Mortality and Graft Failure
associated with the composite outcome of all-cause mortality and graft loss. However, while almost all the studies have shown a significant correlation with graft failure, results regarding the association between anaemia and mortality are still unclear
Cardiovascular Morbidity
Anaemia – independent risk factor for de novo congestive heart failure and left ventricular hypertrophy
eGFR Decline
associated with a decline of GFR and correction of anaemia is associated with a reduction in the rate decline
Diagnostic Evaluation
The classic causes of anaemia as with non transplanted patients
Red blood cell indices,
Reticulocyte counts
Serum iron, total iron-binding capacity (transferrin), percent transferrin
saturation, serum ferritin.
Folate
Vitamin B12
Tests for presence of haemolysis (haptoglobin) when
clinically indicated (elevated reticulocyte counts, lactate
dehydrogenase, and indirect bilirubin).
2. Specific potential causes of anaemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infection
Treatment of PTA
Treatment should be directed at the underlying cause\
Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD and improved death-censored graft survival. Compared to the partial-correction group, the complete-correction group had a smaller decrease in the estimated creatinine clearance (i.e., 5.9 vs. 2.4 mL/
min/1.73 m2), a lower rate of ESRD (i.e., 21 vs. 4.8%), and a higher death-censored graft survival (i.e., 80 vs. 95%). There was also a significant improvement in quality of life in the full-correction group. Regarding cardiovascular outcomes, although the numbers were small, there were no cardiac disorders (cardiac failure, arrhythmia, or myocardial infarction) in the full-correction group compared to 4 patients (8%) in the partial-correction group,
In conclusion, PTA is a common complication of KTRs. It is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anaemia. Treatment of PTA should begin as soon as possible after kidney transplantation. Based on data derived from the CAPRIT study and the observational study by Heinze et al, it appears that the optimal target Hb level in kidney transplant recipients with anaemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. To achieve this target, appropriate treatment with ESA and i.v. iron should be given.
level 4.
Early PTA is usually defined as anemia which develops up to 6 months after transplantation, and late PTA is defined as anemia which develops after 6 months.
In case of early PTA iron deficiency being the major contributor. The occurrence of late PTA has been associated with impaired graft function. Early PTA has been shown to be a predictor of late PTA. PTA is associated with mortality, reduced graft survival, and a decline in GFR.
Post transplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation and negatively associated with the following long-term outcomes: increased rates of al lcause mortality, graft failure, congestive heart failure, left ventricular hypertrophy, and a decline in the estimated glomerular filtration rate
In early PTA Iron deficiency may be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutrition. In addition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
The occurrence of late PTA may be caused by iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir. There is observation that early PTA is a predictor of late PTA as well.
Treatment of PTA should be directed at the underlying cause.
Level 5 evidence
Impact factor can evaluate the importance of a journal. It is calculated by dividing the number of citation in the previous two years by the number of articles published during this time of a journal.
Briefly summarise this article
This article reviews about anemia in kidney transplant recipients after kidney transplantation. The article discusses lot of studies regarding PTA and quotes their observations.
Post transplantation anemia (PTA) is quite common entity and has prevalance to the tune of 20-51% and has deletarious long term outcomes.
PTA has been divided in two categories by some authors.
Causes of PTA
Predictors of PTA
Common deficiencies associated with PTA are, iron deficiency, Vit B12 and folic acid deficiency
Outcomes of PTA
Diagnostic evaluation: Full anemia workup including RBC indices, reticulocyte count, serum iron, TIBC, transferrin saturation, folate levels, etc.
NOTE: Overall this is not a nicely written article. It just keeps quoting articles but doesnt give any consensus statement at the end. There is no summary table of all included articles. There is also error in language
“The Correction of Hemoglobin and Outcomes in Renal Insufficiency
(CHOIR) trial [42] included 1,432 CKD stage
3–4 patients who were randomized to achieve a target Hb
level of 13.5 or 11.3 g/dL using epoetin-α.”
I didnt understand this statement.
What is the level of evidence provided by this article?
Its level 6 evidence as its a narrative review in descriptive format.
What is meant by the impact factor of a journal (please in your own words)?
Impact factor is a sort of method of ranking a journal. It depends on the number of times the articles published in a journal have been cited.
In particular, its the average frequency with which article citation has been done in particular year .
Its calculated as follows:
Number of citations of article (published in last 2 years) in journal citation reports divided by total number of articles published in last 2 years.
Briefly summarize this article
Prevalence of Post-Transplant Anemia (PTA) varies from 20-51%.
Optimal target Hemoglobin after kidney transplant is above 12g/dL in females and 13g/dL in males (WHO, AST criteria).
PTA is divided into two types depending on its occurrence following varying periods after transplant
Early PTA: Anemia within 6 months post-transplant
· Prevalence 50%
· Causes: Iron deficiency anemia (Depletion of iron stores, Peri-operative blood loss, poor nutrition, increase iron utilization with onset of erythropoiesis post transplant)
· Early PTA is a predictor for late PTA
Late PTA: Anemia 6 months post-transplant
· Prevalence:23-35%
· Causes: Nutritional Deficiencies most common cause (Iron deficiency>Vit B12 def>Folate Def), Infections, certain immunosuppressive drugs(MMF, Mycophenolic acid, azathioprine), ACEI, ARB, certain antimicrobials(TMP-SMX) and antivirals like ganciclovir
· Late PTA has been associated with impaired graft function and reduced graft survival
Outcome of Patients with PTA
· Mortality: related to severity of anemia. Severe(<11g/dL) associated with all-cause mortality while mild doesn’t.
· Graft Failure: Anemia is associate with graft failure (Mild as well as severe)
· Cardiovascular morbidity: associated with LVH, de Novo CHF with significant risk of death
· GFR decline: Anemia associated with GFR decline, estimated creatinine clearance and progression to ESRD and correction reverses it
Diagnosis: Following test as same in non-transplant individuals
1. Complete Blood count
2. Reticulocyte count
3. S.Iron
4. S.Ferritin
5. TIBC(Transferrin)
6. Percent Transferrin Saturation
7. S.Folate
8. S.Vit B12
9. Tests for presence of Hemolysis as indicated (Reduced Haptoglobin, Elevated Reticulocyte count, LDH and indirect Bilirubin)
10. Specific Tests for concurrent infection if clinically indicated
Treatment:
· Treat the underlying causes
· Optimal Target level is 12 to 13g/dL
· No specific recommendation present in literature
· Treat it with ESA and oral/IV iron appropriately. IV iron preferred.
· Iron stores to replete before starting ESA
What is the level of evidence provided by this article?
It is Narrative review article and hence level of evidence in 5
What is meant by the impact factor of a journal (please in your own words)?
The impact factor is a measure of frequency with which the average article in a journal has been cited in a particular year.
Calculation is based on a two-year period and involves number of times articles were cited divided by the number of citable articles.
Calculation of 2021 IF of journal:
A=the number of times articles [published in 2019 and 2020 were cited by indexed journals during 2021
B=Total number of citable articles published in 2019 and 2020
A/B=2021 IF of journal
It is used to evaluate the importance or rank of a journal by calculating the times its articles are cited.
The article was a great one and it deals with post-transplantation anemia (PTA). PTA is common in kidney transplant patients with a prevalence of 20-51%. Early PTA is defined as anemia that develops up to 6 months after transplant while late PTA is defined as anemia that develops after 6 months. The optimal target of hemoglobin level in kidney transplant recipients should be about 12.5-13 g/dl.
There are many causes of PTA and depend on if it is early or late.
1) Early PTA
a) Iron deficiency
b) Inadequate iron stores before transplant
c) Blood loss during the procedure
d) Poor diet or nutrition
e) Increase use of EPO
f) Vitamin B 12 deficiency
g) Folic acid deficiency
h) Infections
i) AKI
j) Acute rejection
2) Late PTA
a) Inflammation
b) Infections
c) Iron deficiency
d) Immunosuppressive medications
3) Other causes
a) Due to medications like ACEI, antiviral medications like ganciclovir
b) Nutritional factors
There are predictors of PTA because of females, lower GFR, and hypochromic RBC. It was noted that elevated serum creatinine levels greater than 2mg/dl may be a cause of PTA and is frequent in donors aged above 60 years, medications like ACEI, immunosuppressives like MMF and AZA and infections or sepsis
The outcome of post-transplant patients depends on mortality and graft failure, cardiovascular morbidity, and a decrease in GFR.
HOW DO WE DIAGNOSE A PATIENT WITH PTA
The protocol of anemia is almost like that in patients that are non transplanted. One must study or do the required studies:
1) Haemoglobin levels that are RBC indices and reticulocyte counts
2) Serum iron, TIBC, ferritin, transferrin saturations, etc.
3) Vitamin B12 and folate level
4) Coomb tests
5) Test for hemolysis
6) LDH levels
7) Medications levels like immunosuppressive medications
Treatment of PTA/:
It involves treatment of the cause.
Provide proper nutrition with vitamin B12, folic acid, etc.
Provide EPO or ESA
The article was a level 5
The impact factor of a journal is commonly used to evaluate the relative importance of a journal within its field and to measure the frequency with which the average article in a journal has been cited in a particular period. The higher the IF the better it is for the article.
# Briefly summarise this article
*This review provided updated information regarding the prevalence of post transplantation anemia (PTA) in KT recipients and the causative and predictive factors.
*Early PTA (up to 6 months after transplantation), with prevalence of about 50%.
*Late PTA (after 6 months, and it can appear later up to 8 years later), with prevalence about 23–35%
*The World Health Organization (WHO) criteria and the American Society of Transplantation defined anemia as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men.
*Causes of early PTA is usually due to iron deficiency, due to depletion of iron stores before
Transplantation.
*Perioperative blood loss, and poor nutrition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
*Late PTA is usually associated with impaired graft function and the development of renal insufficiency, other factors are, iron deficiency, inflammation, infection and immunosuppressive drugs (MMF, MPA, AZA, ACE-I, ABBs, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir. Vitamin B12 deficiency was reported to be the cause of PTA in 17–24%, Folic acid deficiency was the cause of anemia in 10%, acute kidney injury in 11.4% of cases, and acute rejection, accounting for 4% of cases. Infections were the cause of anemia in 19% of cases.
# Predictors of PTA included:
female sex, lower eGFR. Factors significantly associated with late PTA and a living donor as the transplantation source was protective.There was a strong association between Hb and graft function, elevated serum creatinine levels > 2 mg/dL, donor age (particularly above 60 years).
# Outcomes of Patients with PTA
# Mortality and Graft Failure
*Study showed that PTA at 12 months was associated with mortality and graft failure. *Prospective cohort study showed PTA to be associated with mortality and graft failure at the 4-year follow-up.
*In a large retrospective analysis it associated with mortality and graft failure at a median follow-up of 6 years.
*Other one reported that PTA at 12 months was associated with an increased risk of death, however, another retrospective conducted that, PTA after 3 months was associated with mortality and graft failure.
# Cardiovascular Morbidity
*A retrospective Canadian cohort study showed that anemia was an independent risk factor for LVH 1–5 years PKT that associated with a significant risk of death, while other conducted, adult renal transplant recipients who were free of cardiac disease 1 year PKT.
# GFR Decline
*Study, showed that anemia is associated with a decline of GFR and it is correction is associated with a reduction in the rate decline.
# Diagnostic Evaluation
*The diagnostic evaluation of renal transplant recipients is the same as non transplanted patients, i.e., red blood cell indices, reticulocyte counts, serum iron, total iron-binding capacity (transferrin), percent transferring saturation, serum ferritin, folate, and vitamin B12, and tests for presence of hemolysis (haptoglobin) when clinically indicated, In addition to test of medications (immunosuppressive and antimicrobial)
*Based on published evidence, a full anemia work-up approximately 3 months post transplantation is indicated as early recognition and treatment may improve the prognosis.
# Treatment of PTA
*Diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause.
*The target Hb level for treatment, followed by the type of treatment, i.e., erythropoiesis-
stimulating agents (ESA) and/or iron, should be determined.
*Anemia (Hb < 12.5 g/dL) was significantly associated with mortality in patients with and without ESA. In patients without ESA, a spontaneous rise in Hb was associated with decreased mortality at any level.
*In patients treated with ESA, improvement of anemia (Hb up to 12.5 g/dL) was associated with decreased mortality as well.
*Further increments in Hb levels led to a tendency toward increased rates of mortality, which became significant at Hb levels > 14 g/dL.
* Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR,and progression to ESRD and improved death-censored graft survival, significant improvement in quality of life, better cardiovascular outcomes, with no cardiac disorders (cardiac failure, arrhythmia, or myocardial infarction)
*The KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL.
*The(NKFKDOQI) guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/Dl.
*No specific recommendation was made for transplant recipients study suggest that the optimal target Hb level in KTR with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL.
*I.V. iron administration after transplantation increased Hb levels and reduced the eGFR decline
*If ESA is initiated, the iron status should be determined and iron stores should be repleted, as with CKD patients.
# What is the level of evidence provided by this article?
Level 5
# What is meant by the impact factor of a journal (please in your own words)?
*The impact factor (IF) is a measure of the frequency with which the average article in a journal has been cited in a particular year. It is used to measure the importance or rank of a journal by calculating the times its articles are cited.
How impact factor is calculated?
* The calculation is based on a two-year period and involves dividing the number of times articles were cited by the number of articles that are citable.
This article by Gvili and Gafter has looked into the causes of anemia and it’s impact on kidney transplant patients.
Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation
Although successful kidney transplantation may correct anemia, up to 20–51% of patients remain anemic after transplantation at various time points
The authors have described anemia into early and late PTA.(late occurring 6 months after transplant)
Early PTA is usually due to iron deficiency. Iron deficiency may be caused by depletion of iron stores before transplantation, perioperative blood loss, and poor nutritionIn in addition, increased iron utilization with the onset of erythropoiesis with slowly increasing levels of the newly graft-produced erythropoietin may contribute to the anemia.
Interestingly one of the predictor of late onset PTA is early PTA.
Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies.
Folic acid deficiency was the cause of anemia in 10% of the cases in the study by this group which is a relatively low rate compared to the 23–41% reported in other studies.
Acute kidney injury and rejection along with infections have also been reported to be cause of PTA.
The authors have concluded by mentioning different studies that PTA is associated with increased mortality , LVH , increased CVS morbidity, decrease in GFR and worst graft outcomes.
The authors suggested that cause of anemia should be ascertained early and managed effectively to avoid its negative impact.
Target Hb in transplant patients should be between 12.5 -13 as shown by CARPIT study.
Level of Evidence is v
Impact factor of journal tells us the relative importance of that journal and it gives us the frequency with which average article in a journal has been cited in a particular time period
Briefly summarise this article
Post transplant anaemia -PTA is an important entity with prevalence between 21-55%. Anaemia is defined as Haemoglobin <12 in females and <13 in males. Anaemia is associated with poor long term graft outcomes, left ventricular failure. Congestive cardiac failure and low eGFR.
This article addresses PTA with prevalence aetiology, prognosis and management.
Prevalence.
Between 21-55% post transplant population.
Early PTA
Anaemia that occurs < 6 months post transplant. It is due to depleted iron stores pre transplant, peri operative losses, nutritional factors. Increased iron utilization by new onset erythropoiesis post transplant.
Late PTA
Anaemia that occurs > 6 months post transplant. This can lead to graft dysfunction . It is usually influenced by graft dysfunction. Other factors like iron deficiency, immune suppressants, ACEi,ARBs antibiotics like trimethoprim and sulphamethoxazole and antiviral may contribute.
Predictors of late PTA cab be living donor, Use of ACEi, ARBi, donor age, infections, low eGFR, female sex
PTA is associated with mortality and poor graft outcome
Treatment of PTA
Identification of underlying cause and then treat that.
Iron replacement
Erythropoiesis stimulating agents
Aim to keep Hb above 12.5g/dl
What is the level of evidence provided by this article?
Review article Level V
What is meant by the impact factor of a journal (please in your own words)?
The impact factor is the tool to assess the importance f a journal and it is based on the number of citations to the article of this journal during specific time period. It calculated by ratio of the number of citations a journal receives in last 2years to the number of publications of that journal in last 2 years. Cites/doc (2 years).
The article from a journal can used as citation in different books , dissertation and presentations. New journal will not have impact factor in first 2 years. So they may not have impact factor in first 2 years . This lead to bias .
This is a Narrative Review – Level 5
It is a paper discussing the causes of post-transplant anemia, specifically in kidney transplantation, dividing into early or late PTA. Another important discussion is the definition of target hemoglobin levels between 12.5 and 13 g/dL.
Early PTA (in the first six months after transplantation) is closely related to iron deficiency. Risk factors include donor age (particularly over 60 years), use of ACE inhibitors or angiotensin receptor blockers, recent infection, or use of immunosuppressants such as MMF and Azathioprine.
Late PTA has early PTA as one of the risk factors, but in these cases, there is an association with kidney injury and graft loss. There are several studies also correlating mortality, but still with conflicting data. However, the impact of anemia on the graft is indisputable. Other deficiencies should be investigated (vitamin B12, folic acid, and nutritional deficiencies).
Cardiovascular morbidity is increased in patients with post-transplant anemia for several reasons, being an independent risk factor for congestive heart failure. Over time, there is a decrease in Creatinine Clearance and consequent loss of the graft.
Treatment is the diagnosis and treatment of all reversible causes (mainly those related to the patient’s nutrition). Erythropoietin stimulators have a well-defined role in the literature, with data showing an improvement in the quality of life of individuals who achieve target hemoglobin. Iron replacement, whether oral or intravenous, plays a crucial role.
The Impact Factor is calculated by dividing the number of citations in the journal citation report per year by the total number of articles published in the two previous years.
Summary :
Definition :
Post transplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation
PTA is not defined uniformly either timing after transplantation or in terms of the degree of anemia:
Early PTA (up to 6 months after transplantation).
Late PTA (after six months)
Anemia in most studies is defined as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men, following World Health Organization (WHO) criteria and the American Society of Transplantation.
Causes of and Predictive Factors for PTA:
Ø Early PTA is usually due to:
1. Iron deficiency
2. Inadequate iron stores at the time of transplantation
3. blood loss during surgery
4. increased iron utilization with the onset of erythropoiesis
5. poor nutrition.
Ø Late PTA is usually due to:
1. iron deficiency
2. inflammation
3. infection
4. immunosuppressive medications
ü Other causes:
Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia.
Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies.
The folic acid deficiency was the cause of anemia in 10% of the cases
Other reasons for PTA included acute kidney injury, acute rejection, and Infections.
üPredictors of PTA:
Factors associated with early PTA included: female sex, lower eGFR, and hypochromic red blood cells
Elevated serum creatinine levels > 2 mg/dL were associated with late PTA.
1-Donor aged above 60 years
2- ACE inhibitors or angiotensin receptor blockers,
3- immunosuppressive drugs such as mycophenolate mofetil and azathioprine,
4- recent infection.
ü Outcomes of Patients with PTA:
1. Mortality and Graft Failure
2. Cardiovascular Morbidity
3. GFR Decline
ü Diagnostic Evaluation:
ü The diagnostic evaluation of renal transplant recipients should include an assessment for “the usual” causes of anemia as with non-transplanted patients
1. Red blood cell indices, reticulocyte counts
2. serum iron, total iron-binding capacity (transferrin), percent transferrin saturation, serum ferritin
3. folate, and vitamin B12
4. tests for the presence of hemolysis (haptoglobin
5. lactate dehydrogenase, and indirect bilirubin
ü Specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial
Treatment of PTA:
ü The management of PTA starts with diagnosing and treating all reversible causes, as therapy should be directed at the underlying cause. However, there is no specific recommendation for treating kidney transplant recipients.
ü Most importantly, the target Hb level followed by the type of treatment, i.e., erythropoiesis-stimulating agents (ESA) and iron, should be determined.
ü The KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL. The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative and targeting (NKFKDOQI) guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/ dL. But, again, no specific recommendation was made for transplant recipients.
· Level 2.
· Impact factor for journal:
The journal impact factor is the number of articles published in the past two years.the impact factor is calculated by dividing the number of citations in the year by the total number of articles published in the two previous years
Impact factors are used to measure the importance of a journal by calculating the number of times selected articles are cited within the last few years.
Post transplant anemia:
Definition of anemia in women less than 12g/dl and male less than 14g/dl.
Early PTA is within 6 months
Late PTA is more than 6 months.
Prevalence of anemia is 20-51% in post transplant.
Early PTA causes mainly IDA results from depletion of iron store before transplant.
Peri operative blood loss
Poor nutrition
Causes of late PTA:
IDA
infection
immunosuppressive drug
Post transplant anemia assess with decrease graft function and decline eGFR and left ventricle hypertrophy and congestive heart failure.
Predictor of late PTA:
early PTA
serum creatinine level more than 2mg/dl
Age more than 60y
Medication like ACEI / ARBS/ azathioprine and septrin and valgancyclovir
Aetiology and incidence according to retrospective study done between 2000-2016 in rabin medical center.
IDA 13%
nutritional deficiency
Vit B12 deficiency 17-24%
Folic acid deficiency 10%
AKI 11.4%
Acute rejection 4%
Infection 19%.
Outcome of patients with PTA:
Anemia associated with graft loss and progressive decline in eGFR.
There’s no evidence of anemia increase mortality but it’s depend on severity of anemia.
Anemia is independent risk of LVH and de novo congestive heart failure.
Diagnosis of PTA:
RBC indices
Reticulocyte count
S.iron / TIBC/ ISR/ S. ferritin , folate and vit B12.
S. haptoglobin , LDH, indirect bilirubin.
Evaluation of medication: Immunosuppressive therapy and antimicrobial agents contribute to anemia.
So early recognition and early treatment improve graft function.
Management:
Treatment of underlying cause
Intravenous iron
ESA
Anemia is defined as haemoglobin less than 12 g/dl in women and <13 g/dl in men. Kidney transplant patients develop post-transplant anemia (PTA) with the incidence rates ranging from 20% to 51%. Early PTA (within 6 months post-transplant) occurs in upto 50% while the incidence of late PTA ranges from 23-35%. PTA has been shown to be associated with increased rates of all-cause mortality, graft failure, congestive cardiac failure, left ventricular hypertrophy and fall in GFR.
Early PTA is usually caused due to iron deficiency while late PTA is caused due to reduced graft function, iron deficiency, vitamin B12 and folic acid deficiency, inflammation, infection, and medications including immunosuppressants (like MMF and azathioprine), ACE inhibitors, Angiotensin receptor blockers, trimethoprime-sulfamethoxazole and ganciclovir. Other causes of PTA include AKI and acute rejection. Predictors of PTA include recent infection, donor age more than 60 years, use of ACE inhibitors and ARBS, MMF and azathioprine. Predictors specific for early PTA include female gender, lower GFR and hypochromic RBCs. Predictors for late PTA include early PTA, non-living donor, female gender and increased serum creatinine at 3-month post-transplant.
Studies analysing outcomes with PTA with respect to mortality show increase in mortality by 69%, more with severe anemia (hemoglobin<11 g/dl). This increase is not seen with mild anemia. The incidence of graft failure increases by 2.46 times and GFR falls by 5.26 ml/min/1.73m2 between 6 and 24 months post-transplant. PTA is associated with increased left ventricular hypertrophy and CCF leading to increased mortality.
The diagnostic evaluation of PTA involves a full anemia work-up at 3 months post-transplant including RBC indices, reticulocyte count, peripheral blood film, serum iron, TIBC, ferritin and transferrin saturation, serum vitamin B12, folic acid and haptoglobulin levels.
Management of PTA includes diagnosis and treatment of all reversible causes of anemia. Hemoglobin <12.5 g/dl has been shown to be associated with increased mortality. Correction of PTA using erythropoietin has been shown be associated with better graft survival and quality of life (CAPRTI trial). Similar correction of anemia in CKD patients has not shown delay in progressive renal failure and has been shown to be associated with increased cardiovascular events (CHOIR and TREAT trial).
Based on these data, KDIGO recommends use of erythropoietins in CKD only if hemoglobin is less than 10 with target of 11.5g/dl. Optimal target hemoglobin in kidney transplant recipients is 12-13g/dl. Intravenous iron use in transplant recipients has been shown to increase hemoglobin levels and decrease the eGFR fall. Iron stores should be replenished before starting erythropoietins. In early PTA management, both oral and intravenous irons are equally efficacious with respect to time required to achieve hemoglobin of more than 11g/dl. Intravenous iron use is safe in transplant recipients.
The level of evidence is Level 5 – narrative review.
Impact factor of a journal is the average number of citations received by each article published in that journal in the previous 2 years. It is a number derived by dividing the total number of citations received by total number of articles published in the journal.
Reference:
Sharma M, Sarin A, Gupta P, Sachdeva S, Desai AV. Journal impact factor: its use, significance and limitations. World J Nucl Med. 2014 May;13(2):146. doi: 10.4103/1450-1147.139151. PMID: 25191134; PMCID: PMC4150161.
IV. Posttransplantation Anemia in Kidney Transplant Recipients
Introduction
Posttransplantation anemia (PTA) is common among kidney-transplant patients, with a prevalence of 20–51% at various time points after transplantation. It has been shown to be negatively associated with:
1. Increased rates of all cause mortality.
2. Graft failure
3. Congestive heart failure.
4. Left ventricular hypertrophy.
5. Decline in the estimated glomerular filtration rate (eGFR).
Prevalence and Epidemiology
Although successful kidney transplantation may correct anemia, up to 20–51% of patients remain anemic after transplantation at various time points.
Two main types:
1. Early PTA (up to 6 months after transplantation), occurs in 50% of cases.
2. Late PTA (after 6 months), occurs in 23-35%.
Defined as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men, in accordance with World Health Organization (WHO) criteria and the American Society of Transplantation.
Causes of and Predictive Factors for PTA
1-Early PTA is usually due to iron deficiency.
2-ate PTA has been associated with impaired graft function
and the development of renal insufficiency. Late PTA is predominantly influenced by a reduced allograft function. However, other factors, i.e., iron deficiency, inflammation and infection, immunosuppressive medications (Mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia
Predictors of PTA
In retrospective study, predictors of early PTA included:
· Female sex.
· Lower eGFR.
· Hypochromic red blood cells
Factors significantly associated with late PTA (2 years after transplantation) included:
· Early PTA, (HR 0.601; 95% CI 0.453–0.799, for every
· Living donor as the transplantation source was protective
· Donor age (particularly above 60 years).
· Use of ACE inhibitors or angiotensin receptor blockers.
· Use of immunosuppressive drugs such as mycophenolate mofetil and azathioprine.
· Recent infection.
Etiology of PTA
· Iron deficiency is the most common contributing factor for early PTA.
Reasons for that include:
1. Inadequate iron stores at the time of transplantation.
2. Blood loss during surgery.
3. Increased iron utilization with the onset of erythropoiesis.
4. Poor nutrition
· Vitamin B12 deficiency was reported to be the cause of PTA in 17–24% of patients in several studies.
· Folic acid deficiency was the cause of anemia in 23-41%
· Acute kidney injury, accounting for 11.4% of cases, and
· Acute rejection, accounting for 4% of cases.
· Infections were the cause of anemia in 19% of cases.
Outcomes of Patients with PTA
Mortality and Graft Failure
PTA has previously been shown to be associated with the composite outcome of all-cause mortality and graft loss. However, while almost all of the studies have shown a significant correlation with graft failure, results regarding the association between anemia and mortality are inconsistent..
Cardiovascular Morbidity
Anemia was identified as an independent risk factor for de novo congestive
heart failure and left ventricular hypertrophy in retrospective studies.
GFR Decline
Anemia is associated with a decline of GFR and correction of anemia is associated with a reduction in the rate decline.
Diagnostic Evaluation
The diagnostic evaluation of renal transplant recipients should include an assessment of :
1. The usual” causes of anemia as with nontransplanted patients.
Red blood cell indices,
Reticulocyte counts
Serum iron, total iron-binding capacity (transferrin), percent transferrin
saturation, serum ferritin.
Folate
Vitamin B12
Tests for presence of hemolysis (haptoglobin) when
clinically indicated (elevated reticulocyte counts, lactate
dehydrogenase, and indirect bilirubin).
2. Specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications (immunosuppressive and antimicrobial), concurrent infections, etc., should be sought.
Treatment of PTA
Treatment should be directed at the underlying cause. However,
there is no specific recommendation for the treatment of kidney transplant recipients. Questions to be addressed are target Hb and weather to give and /or ESA.
Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD and improved death-censored graft survival. Compared to the partial-correction group, the complete-correction group had a smaller decrease in the estimated creatinine clearance (i.e., 5.9 vs. 2.4 mL/
min/1.73 m2), a lower rate of ESRD (i.e., 21 vs. 4.8%), and a higher death-censored graft survival (i.e., 80 vs. 95%). There was also a significant improvement in quality of life in the full-correction group. Regarding cardiovascular outcomes, although the numbers were small, there were no cardiac disorders (cardiac failure, arrhythmia, or myocardial infarction) in the full-correction group compared to 4 patients (8%) in the partial-correction group,
In conclusion, PTA is a common complication of renal transplant recipients. It is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anemia. Treatment of PTA should begin as soon as possible after kidney transplantation. Based on data derived from the CAPRIT study and the observational study by Heinze et al, it appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
This is a review article level 4.
Impact factor (IF) is used to assess the relative importance of a journal within its field and to measure the frequency with which the “average article” in a journal has been cited in a particular time period. Journal which publishes more review articles will get highest IFs. Impact factor can’t be calculated for journal unless it completes 3 years of publications.
The problems with IF, it reflects the number of citations which may not always reflect how good is the journal. Second thing journal which publishes more review articles will get high IF and journal which publishes more original articles, which may be landmarks in the field may get lower IF. Lastly IF reflects 2 years only of the journal not the whole duration of its life.
Formula of IF = total citations of all articles in previous 2years/number of articles published in same 2years period
Briefly summarize this article
According to WHO and AST, anemia is defined as hemoglobin levels < 12 g/dL in women and < 13 g/dL in men.
Two types of anemia are recognized post-transplantation
– Early post-transnsplanty anemia- up to 6 months after transplantation, prevalence is about 50% according to various studies. It is usually caused by iron deficiency from blood loss during surgery or delay graft function.
– Late PTA after 6 months- with prevalence of 23–35%. Usually due to progressive decline in kidney function- chronic allograft nephropathy. PTA is associated with increased risk of cardiovascular mortality and worsening of kidney function.
Etiology of PTA:
Iron deficiency is the most common cause of PTA in the early post-transplantation period. Low iron stores post-operatively is linked to blood loss during surgery, poor nutrition and inflammatory state which decreases utilization of iron into bone marrow.
Vitamin B12 deficiency
Folic acid deficiency
AKI
Acute rejection,
Infections
Outcomes of Patients with PTA
Mortality and Graft Failure
PTA was shown to be associated with increased all-cause mortality and graft loss, as reported in some studies. However, other studies fail to show an association with mortality risk, but a significant association with graft loss was demonstrated. Anemia is an independent risk factor for LVH and heart failure.Anemia is associated with worsening of kidney function, and correction of anemia is associated with a reduction in the rate decline.
Diagnostic Evaluation
RBC indices, Retic counts, serum iron, TIBC, Ferritin, vitamin B12, folic acid, hemolytic workup and stool occult blood gor GI losses
Treatment of PTA
Treatment should be focused on the underlying reversible causes.
KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL.
The optimal target of Hb in kidney transplant recipients was suggested to be 12-13 g/dl .
What is the level of evidence provided by this article?
Level 2
What is meant by the impact factor of a journal (please in your own words)?
Impact factor is calculated by dividing the number of citations of the journal by the the sum of its citable publications during the previous two consecutive years.
Post transplant anemia PTA is commonly encountered in our daily practice. This article, elaborately discussed the subject, detailing its etiology, causes, classification, risk factors, outcome and comparing different studies conducted to address this issue.
definition of anemia :
HB below 13 in male and below 12 in female.
Early PTA , diagnosed within 6 months post transplantation, incidence around 50 %.
Late PTA anemia diagnosed after 6 months of kidney transplantation.
Etiology:
Most common cause of early PTA is Iron deficiency secondary to pretransplant depletion of Iron store, peri-transplant blood loss and the escalating endogenous level of allograft produced Erythropoietin consuming the matched iron store.
Risk factors:
female patients, low GFR, iron store.
For late PTA main risk factors are Iron deficiency anemia, GFR, life donor vs cadaveric donors, chronic kidney disease and allograft failure.
Furthermore, medications related, mainly MMF, valgancyclovir, TMS, CNI, and Renin inhibitors like ACEi.
Several studies were reviewed, showcasing the argumantative impact of anemia on mortality rate and progression of allograft failure, highlighting the debate on this contentious issue, Increased mortality was attributed to LVH.
Treatment was directed towards the underlying etiological factor, basically Iron replacement and ESA therapy. with target HB depend on GFR and the presence of allograft dysfunction.
however, it was not clear what is the indication to start ESA post transplantation as there is no consensus on this issue. Nevertheless, extrapolating the recommendation of KDOGI guideline on the time and threshold for initiating iron and ESA therapy.
I have published a case report discussing the same issue few years back , I am sharing here with you.
The level of evidence is 4 as its a narrative paper.
Impact factor: in my humble language and understanding it is how popular and well known is the journal with how many subscribers and citations made over a period of time
Briefly summarise this article
Post-transplantation anemia (PTA) is common among kidney-transplant patients. There is the early PTA which is (up to 6 months after transplantation) with a prevalence of around 50% and late PTA (after 6 months) with around 23-35%.
Causes of PTA
Early PTA:
Iron deficiency is the most common contributing factor for early PTA
Inadequate iron stores at the time of transplantation blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition all contribute to the occurrence of iron deficiency
Late PTA:
Can appear as late as up to 8 years. Late
PTA is predominantly influenced by a reduced allograft function.
Other factors:
iron deficiency
inflammation and infection
Medications: immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin- aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such as trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir.
Other Causes for PTA:
Vitamin B12 deficiency
Folic acid deficiency
Acute kidney injury
Acute rejection
Predictors of PTA
female sex
lower eGFR
Hypochromic red blood cells
Early PTA (for the late PTA)
a living donor
donor age > 60
Medications: ACEi or ARBs MMF and azathioprine
Recent Infection
a recent infection.
early PTA is a predictor of late PTA
Outcomes of Patients with PTA
· Mortality and Graft Failure
PTA has previously been shown to be associated with the composite outcome of all-cause mortality and graft loss, though results about mortality are inconsistent.
However, overall, in certain studies. the association between anemia and mortality was related to severity. Severe anemia (Hb <11 g/dL) was consistently associated with mortality while mild anemia was not. Both severe and mild anemia were associated with graft failure.
· Cardiovascular Morbidity
Anemia is considered as an independent risk factor for left ventricular hypertrophy & de novo congestive heart failure.
· GFR Decline
Anemia is associated with a decline of GFR and correction of anemia is associated with a reduction in the rate decline.
Diagnostic Evaluation
· red blood cell indices
· reticulocyte counts
· serum iron, total iron-binding capacity, transferrin saturation
· serum ferritin, folate, and vitamin B12
· haptoglobin
· lactate dehydrogenase
· Indirect bilirubin
In addition, potential causes of anemia should be sought.
Treatment of PTA
Treatment should be directed at the underlying cause
Erythropoiesis-stimulating agents (ESA) and/or iron, should be determined.
KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is <10.0 g/dL, with a target Hb level of 11.5 g/dL based on landmark trials (CHOIR, TREAT, CREATE).
The CAPRIT trial, however, which was done in transplanted patients is smaller than all of previous trials and it is also limited by its short duration of 2 years. Nevertheless, it is the only randomized controlled trial (RCT) addressing this question in the transplanted population.
The results of this study as well as those of another large observational study suggest that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL.
It seems reasonable to treat with ESA and/or IV iron if indicated in transplanted patients.
What is the level of evidence provided by this article?
Evidence from systematic reviews of descriptive and qualitative studies (meta-synthesis).
What is meant by the impact factor of a journal (please in your own words)?
It is a measure to evaluate the importance of a journal within its field and this can be assessed by the number of its citations over a 2-year period.
It can be calculated after completing the minimum of 3 years of publication. Therefore, impact factor cannot be calculated for new journals.
The disadvantage is the misuse in evaluating individuals is it depend upon personal judgments.
Post transplant anemia is a common complication of renal transplant recipients. Prevalence is 20- 50% at various time points after transplantation.
PTA is associated with increased mortality, reduced graft survival and a decline GFR.
Anemia is defined as Hb level <12 g/dl in women and <13g/dl in men.
Early PTA is defined as anemia which develops upto 6 months after transplantation and late PTA is defined as anemia which develops after 6 months.
Causes
Early PTA is usually due to iron defeciency.
Late PTA has been associated with impaired graft function and the development of renal insuffiency. Hoever other factors like iron defeciency, inflammation,infection, immunosuppressive medications, ACE inhibitors, ARB, trimethoprim – sulfamethoxazol and anti viral agents ganciclovir may causes anaemia.
Diagnostic evaluation:
Red cell indices, reticulocyte counts, s iron, TIBC, s. ferritin, folate, vitamin B 12, and tests for hemolysis when indicated.
Management
Starts with diagnosis and treatment of all reversible causesBased on data from CAPRIT is upto 12. 5 to 13 g/dl. Appropriate treatment withESA i.v iron should be given
☆ Summary: Posttransplantation Anemia in Kidney Transplant Recipients (KTR)
▪︎This review provided updated information about the prevalence of PTA in KTR and the causative and predictive factors.The effect of anemia on long-term outcomes & treatment options.
▪︎Introduction
Post-transplantation anemia (PTA) is common among KTR & is negatively associated with the following long-term outcomes: increase mortality rate, graft dysfuction, congestive heart failure, LVH, and a decline in the (eGFR).
▪︎Prevalence:
– Up to 20–51% of patients remain anemic at various time points post transplantation.
– Two types of PTA are distinguished early (up to 6 months after transplant with prevalence about 50%) and late (after 6 months in 23–35%).
▪︎Predictors of PTA
– Female sex, lower eGFR, and hypochromic red blood cells.
– Factors significantly associated with late PTA (2 years after transplantation) included early PTA, and a living donor. TRESAM showed a strong association between Hb and graft function; Elevated serum creatinine levels >2 mg/dL were associated with late PTA.
– Other factors that were associated with PTA included: donor age (particularly above 60 years), the use of ACE I or ARB, the use of immunosuppressive drugs such as MMF & azathioprine, and a recent infection.
– The observation that early PTA is a predictor of late PTA.
Etiology of PTA
– Iron deficiency is the most common contributing factor for early and late PTA due to: inadequate iron stores at the time of transplantation, blood loss during surgery, increased iron utilization with the onset of erythropoiesis, and poor nutrition.
– Common causes of late PTA were nutritional deficiencies (Iron &Vitamin B12, Folic acid)
– Other causes of PTA: acute kidney injury, acute rejection and infections.
Outcomes of Patients with PTA:
1. Mortality & Graft Failure.
2. Cardiovascular Morbidity (LVH & CHF).
3. GFR Decline
Diagnostic Evaluation
– Should include: an assessment for “the usual” causes of anemia. In addition to, specific potential causes of anemia that may be unique to renal transplant recipients, such as the use of medications, concurrent infections, etc., – Early recognition & treatment may improve the prognosis.
Treatment of PTA
– Should be directed to the underlying cause.
– There is no specific recommendation for the treatment of kidney transplant recipients.
– Treatment should target Hb level, followed by the type of treatment, i.e., erythropoiesis-stimulating agents and/or iron, should be determined.
– A study showed that: normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β can reduce the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD, improved graft survival, improvement in quality of life and no cardiac disorders.
– The KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is <10.0 g/dL, with a target Hb level of 11.5 g/dL.
– The NKFKDOQI guidelines commented on these guidelines and endorsed the FDA-recommended upper cut-off of 11 g/ dL.
– The optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12–13 g/dL ( according to CAPRIT trial and large observational study by Heinze et al).
– Iron deficiency, even without anemia, has been shown to be an independent predictor of mortality in KTR. However, i.v. iron administration after transplantation increased Hb levels and reduced the eGFR decline.
– If ESA is initiated, the iron status should be determined and iron stores should be repleted, as with CKD patients.
– It is unclear in the transplant setting whether i.v. iron is better than orally administered iron. But according to study results, it seems reasonable to treat transplanted patients with i.v. iron.
Conclusion
– PTA is associated with reduced mortality (which is related to severity of anaemia), reduced graft survival, and a decline in GFR.
– Treatment of PTA should begin as soon as possible after renal transplantation. – Based on data derived from the CAPRIT and study and the observational study by Heinze et al., it appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. To reach this target, appropriate treatment with ESA and i.v. iron should be given.
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Introduction
– Post transplantation anemia (PTA) is common among
kidney-transplant patients.
-A prevalence of 20-51% after transplantation.
– Early PTA is anemia usually develops up to 6 months after transplantation, and late anemia which develops after month.
– PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR and association with mortality is related to the severity of the anemia and to specific causes of anemia.
-The following long-term outcomes: –
*increased rates of all-cause mortality , graft failure , conges tive heart failure , left ventricular hypertrophy ,
and a decline in the estimated glomerular filtration rate (eGFR) .
– The optimal target hemoglobin level in kidney transplant recipients up to 12.5–13 g/dL.
Prevalence and Epidemiology
-Although successful kidney transplantation may correct anemia, up to 20–51% of patients remain anemic after transplantation at various time points.
-Anemia in most studies is defined as hemoglobin (Hb)
levels < 12 g/dL in women and < 13 g/dL in men, in accor-dance with World Health Organization (WHO) criteria
and the American Society of Transplantation.
– The prevalence of early PTA is about 50% and 23-35% late PTA.
Causes of and Predictive Factors for PTA
–
-Early PTA is usually due to iron deficiency.
– Late PTA is usually defined as anemia that occurs
more than 6 months after transplantation, and it can ap-
pear as late as up to 8 years later.
-late PTA has been associated with impaired graft func-
tion and the development of renal insufficiency.
– Late PTA is predominantly influenced by a reduce allograft
function.
– Other factors, include iron deficiency, inflammation and infection, immunosuppressive medications (mycophenolate mofetil, mycofenolic acid, and azathioprione), medications affecting the renin-angiotensin-aldosterone system such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, antimicrobial agents such trimethoprim-sulfamethoxazole, and antiviral agents such as ganciclovir, may contribute to the anemia .
Etiology of PTA
The most common contributing factor for early PTA:-
1- Iron deficiency (34.7%)
2- Inadequate iron stores at the time of transplantation
3- Blood loss during surgery
4- Increased iron utilization with the onset of erythropoiesis
5- And poor nutrition all contribute to the occurrence of iron deficiency.
6- 61% late PAT (poor nutrition)
7- Vitamin B12 deficiency was cause of PTA in 17–24% .
8- Folic acid deficiency was the cause of anemia in 10%
Outcomes of Patients with PTA
1- Mortality and Graft Failure
2- Cardiovascular Morbidity
3- GFR Decline
-A retrospective multicenter analysis using aFrench database that included 4,217 transplant recipients.
-showed that PTA at 12 months was associated with mortality and graft failure.
– A retrospective multicenter analysis using a French database that included 4,217 transplant recipients.
– A prospective cohort study of 938 kidney transplant recipients in Hungary showed PTA to be associated with mortality and graft failure at the4-year followup.
-In a large retrospective analysis of 2,031 transplant recipients in Austria, anemia was significantly associated with mortality and graft failure at a median follow-up of 6 years – A retrospective series of 626 transplant recipients in Pennsylvania, USA, reported that PTA at 12 months.
IN all of these studies PTA was significantly assaciated with mortality and graft loss .
–In the other study , the association between anemia and mortality was related to severity.
–Severe anemia (Hb < 11 g/dL) was consistently associated with mortality, while mild anemia was not.
–Both severe and mild anemia were associated with graft failure.
Diagnostic Evaluation
The diagnostic evaluation of renal transplant recipients should include:
– Red blood cell indices,
-Reticulocyte counts,
– Serum iron, TIBC
-TSAT%,
-Serum ferritin,
-Folate, and vitamin B 12
-Thyroid function tests – And hemolysis (haptoglobin) when (elevated reticulocyte counts, lactaedehydrogenase, and indirect bilirubin).
Treatment of PTA
1- The management of PTA starts with diagnosis and
treatment of all reversible causes.
2-Treatment should be directed at the underlying cause.
3-There is no specific recommendation for the treatment of
kidney transplant recipients .
4- Most importantly, the target Hb level for treatment, followed by the type of treatment, i.e., (ESA) and/or iron, should be determined.
5- In the CAPRIT trial mentioned above higher Hb levels were associated with graft survival and in this trial, 125 renal transplant recipients were randomly assigned to re-
ceiving epoetin-β with a target of 13–15 g/dL (complete correction group) or 10.5–11.5 g/dL (partial correctio group).
6- Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR,and progression to ESRD and improved death-censored graft survival.
7-The optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL.
8- In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
Conclusion
PTA is a common complication of renal transplant recipients associated with reduced mortality, reduced graft survival, and a decline in GFR.
Treatment of PTA should begin as soon as possible after kidney transplantation.
CAPRIT study and the observational study by Heinze et al. it appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL.
In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
· What is the level of evidence provided by this article?
The level V
· What is meant by the impact factor of a journal (please in your own words)?
Impact factor of a journal = Total number of times its articales were cited during the two previous years ÷ Total number of citable articales in the journal during those two years.
Posttransplantation anemia (PTA) is common among kidney transplant patients.
divided into two types
optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL.
Prevalence and Epidemiology
up to 20–51% of patients remain anemic after transplantation.
The prevalence of early PTA is about 50% and the prevalence of late PTA declines to about 23–35% at various time points up until 8 years after transplantation.
Causes of and Predictive Factors for PTA
Early PTA
late PTA
Predictors of PTA
early PTA
late PTA
Outcomes of Patients with PTA
Diagnostic Evaluation
Treatment
there is no specific recommendation for the treatment of kidney transplant recipients
Most importantly, the target Hb level for treatment, followed by the type of treatment, i.e., erythropoiesis-stimulating agents (ESA) and/or iron, should be determined.
In the CAPRIT trial mentioned abovehigher Hb levels were associated with graft survival.
Normalization of PTA (complete correction to Hb levels of 13–15 g/dL) with epoetin-β reduced the rate of decline of the estimated creatinine clearance, the eGFR, and progression to ESRD and improved death-censored graft survival.
If ESA is initiated, the iron status should be determined and iron stores should be repleted, as with CKD patients.
It appears that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with ESA and i.v. iron should be given.
What is the level of evidence provided by this article?
level of evidence V
What is meant by the impact factor of a journal ¿
Impact factor is commonly used to evaluate the relative importance of a journal within its field and to measure the frequency with which the “average article” in a journal has been cited in a particular time period.
Post transplantation anemia (PTA) is common among kidney transplant patients.
1- Early PTA : anemia which develops up to 6 months after transplantation
2- Late PTA : anemia which develops after 6 months
The prevalence of early PTA is about 50% and the prevalence of late
PTA declines to about 23–35% at various time points up until 8 years after transplantation
PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR.
Treatment of PTA should probably begin as soon as possible after kidney transplantation
The optimal target hemoglobin level in kidney transplant recipients should be up to 12.5–13 g/dL.
Causes of PTA :
1- Early : Iron deficiency anemia
2- Late :
Outcomes of Patients with PTA
Diagnostic Evaluation
The management of PTA starts with diagnosis and treatment of all reversible causes. As such, treatment should be directed at the underlying cause with HGB level of 12.2 – 13 . However, there is no specific recommendation for the treatment of kidney transplant recipients
What is the level of evidence provided by this article?
level of evidence V.
What is meant by the impact factor of a journal (please in your own words)?
The impact factor of a journal in a period of time means how many citations in a given period of time to number of citable articles in the journal, journals with high impact factor more stronger than those with low one.
thanks
Summarize the article
Introduction
Anemia post kidney transplantation is common and varies in prevalence between 20-51%at different points times (1-4).
Post kidney transplant anemia (PTA) can be classified as early PTA in the first 6 months which could be multifactorial including IDA,
Late PTA after 6 months which usually associated with graft dysfunction, infection, rejection, malignancy, and drug effect. According to the WHO criteria and American transplant criteria, anemia is defined by a low HB level of < 12 gm in females, and < 13 gm in males Early PTA is more prevalent and reported up to 50% as per the evidence from many studies, its more of IDA due to surgical blood loss and depletion of the iron store, poor nutrition pre-transplantation period also due to increased iron utilization with increased erythropoiesis. While late PTA in the range of 23-35% in different time points up to 8 years after transplantation, usually associated with reduced graft function, infection, inflammation with IDA, drug effects like MMF, AZATHIOPRINE, ACEI, ARBS, antibiotics like trimethoprim and antiviral like ganciclovir. Early PTA is the most prognosticator of late PTA, PTA is associated with higher mortality and morbidity. The more severe degree and type of anemia can affect the graft function with reduced GFR and lower survival rate, so anemia post-transplantation should be addressed and treated promptly with epoetin (ESA) and iron supplement, targeting a higher level of HB in the range of 12-13gm.
Predictors for PTA:
Early PTA
1. Female sex
2. Lower GFR
3. percentage of hypochromic RBCs
Late PTA
1. Early PTA
2. Living donor source for KTX was protective
3. donor age > 60 years
4. use of ACEI, ARBS, MMF, azathioprine
5. recent infection
AIM of this study
1- To give an update on the prevalence of PTA
2- Determine the risk factors
3- Address the mortality and morbidity of PTA
4- Determine the PTA effect on long-term outcome
5- Debate treatment opportunities
Method and setting of this study:
a large retrospective cohort from a single tertiary center in Israel (RMC) included > 1135 KTX recipients with 4 years FU.
Period of the study 2002-2016
Results:
Prevalence of PTA of 36%, and IDA due to nutritional deficiency contribute to most of the causes of early PTA
AKI in 11.3 %, acute rejection in 4%, infection in 19%, lower rate of folic acid deficiency was found in 10% (compared to 23-41% in other studies)
PTA is associated with reduced GFR by 2.6ml/min/1.73m2, similar to finding in other studies like CARPET Trails, and correction of anemia prevents GFR decline rate.
The majority of studies from a diverse population show conflicting results regarding the PTA and the mortality risk however majority confirm the association between PTA and graft failure. Only severe anemia was associated with increased HR of mortality while mild and severe anemia were both associated with graft failure in this cohort study and this might explain the conflicting results from other studies.
Cardiovascular morbidity
Again, PTA is associated with increased cardiovascular risk, and based on many studies PTA consider an independent risk of LVH, LVF, and cardiac death
Management of PTA
The investigation includes the same approach for anemia work up, in general, including the RBCs indices and iron profile transferrin binding, IBC, and ferritin, in certain conditions will do hemolytic markers like LDH, PERIPHERAL SMEAR, indirect bilirubin, and haptoglobin, B12, Folate, viral infection screen like CMV, EBV, parvoviral 19
Early treatment of PTA by targeting the underlying cause and use of iron replacement and ESA with target higher level of HB 12.5-13gm based on data from CARPET trial and Heinz et al observational study.
IV. Posttransplantation Anemia in Kidney Transplant Recipients
Briefly summarise this article
Definitions
Early PTA: up to 6 months post transplantation
Late PTA: after 6 months
Anemia (WHO & the AST definition):
Hb <12 g/dL in women & < 13 g/dL in men.
Prevalence
Early PTA: 50%
Late PTA: 23–35%
Causes:
Early PTA is due to iron deficiency (ID).ID is due to depletion of iron stores before transplantation, perioperative blood loss, poor nutrition, & increased iron utilization with the onset of erythropoiesis with increasing levels of the newly graft-produced erythropoietin.
Late PTA is usually associated with impaired graft function & the development of renal insufficiency. Other factors include: ID, inflammation & infection, IS medications
(MMF, MPA, & azathioprione),RAS blockers, & antimicrobials (e.g. septrin & ganciclovir)
Vitamin B12 deficiency causes PTA in 17–24% of patients.Folic acid deficiency is responsible for 10% of cases of PTA.
Other causes include AKI & acute rejection.
Predictors of PTA
Include:
Female sex
Early PTA is a predictor of late PTA.
A living donor as the transplantation source is protective.
There is a strong association between Hb & graft function. Elevated creatinine levels
> 2 mg/dL are associated with late PTA.
Donor age (particularly above 60 years)
Outcomes of Patients with PTA Mortality & Graft Failure
PTA at 12 months was associated with mortality & graft failure (French database, 4,217 transplant recipients).
PTA associated with mortality & graft failure at the 4-year follow-up (A prospective cohort study of 938 recipients in Hungary).
Anemia was significantly associated with mortality & graft failure at a median follow-up of 6 years(a large retrospective of 2,031 recipients in Austria).
PTA at 12 months was associated with an increased risk of death (A retrospective of 626 recipients in Pennsylvania, USA, reported that).
PTA after 3 months was associated with mortality & graft failure (retrospective of 1,023 recipients in Chicago, IL, USA).
The authors showed that PTA was associated with increased mortality at 2 years in 266 transplant recipients.
In a more recent study of 1,139 patients, PTA at any time point (6–18 months after transplantation) was associated with the composite endpoint of mortality & graft failure, as well as with each of the components.
In a retrospective European study of 825 recipients, PTA was not associated with all-cause mortality with a follow-up of 8 years.
Hb levels were not associated with any effect on cardiovascular morbidity or mortality at a 5- to 6-year follow-up (cohort of 2,102 Danish transplant recipients).
PTA at 12 months was not associated with mortality (a retrospective Chinese study of 887 recipients,).
In all of these studies anemia was significantly associated with graft loss.
Other studies failed to show an association with all-cause mortality, but a significant association with graft loss was reported.
The author reported that severe anemia
(Hb < 11 g/dL) was consistently associated with mortality, while mild anemia was not. Both severe & mild anemia were associated with graft failure.
Cardiovascular Morbidity
Anemia is an independent risk factor for LVH 1–5 years after transplantation (Canadian cohort of 473 recipients). LVH & anemia were associated with a significant risk of death.
Anemia was an independent risk factor for de novo CHF in another retrospective Canadian cohort of 638 recipients.
GFR Decline
There was a decline of eGFR with time in patients with PTA. There was a difference of 5.26 mL/min/1.73 m2 in eGFR between
6 months & 2 years.
Normalization of PTA to an Hb level of 13–15 g/dL reduced the rate of decline of eGFR, progression to ESRD, and improved death-censored graft survival(CAPRIT trial).
Diagnostic Evaluation
Should include:
-Red blood cell indices
-Reticulocyte counts
-Serum iron, TIBC, percent transferring saturation, & serum ferritin
-Serum folate & vitamin B12
-Tests for presence of hemolysis (haptoglobin, elevated reticulocyte counts, LDH, & indirect bilirubin).
Search for specific causes of PTA that may be unique to transplant recipients:
-Medications (IS & antimicrobial)
-Concurrent infections
-Based on evidence, a full anemia work-up 3 months post transplantation is indicated as early recognition & treatment may improve the prognosis.
Treatment of PTA
Treat the underlying cause.
No specific recommendation for the treatment of kidney transplant recipients.
Anemia (Hb < 12.5 g/dL) was significantly associated with mortality in patients with & without ESA (study of 1,794 recipients in Austria, between 1992 &2004).
In patients without ESA, a spontaneous rise in Hb was associated with decreased mortality at any level.
In patients treated with ESA, improvement of anemia (Hb up to 12.5 g/dL) was associated with decreased mortality as well.
Further increments in Hb levels led to a tendency toward increased rates of mortality, which became significant at
Hb levels > 14 g/dL.
Normalization of PTA (Hb levels of 13–15 g/dL) with epoetin-β reduced the rate
of decline of the estimated creatinine clearance, the eGFR, & progression to ESRD & improved death-censored graft survival.
Quality of life also improved with full correction.
There were no cardiac disorders (HF, arrhythmia, or MI) in the full-correction group.
Both the CHOIR trial & the TREAT reported an increased risk of CV events & no delay in progressive renal failure by targeting normalization of Hb with ESA therapy.
CREATE trial showed that randomization to a higher Hb target significantly increased the likelihood of initiation of chronic dialysis.
KDIGO guidelines recommend initiating ESA in patients with CKD only when the Hb concentration is < 10.0 g/dL, with a target Hb level of 11.5 g/dL.
The NKFKDOQI guidelines endorsed the FDA-recommended upper cut-off of 11 g/
dL. No specific recommendation was made
for transplant recipients.
The CAPRIT trial in transplanted is the only RCT addressing this question in the transplanted population. The results suggest that the optimal target Hb level in kidney transplant recipients with anemia is higher than the target suggested in CKD & should probably be up to 12–13 g/dL.
A larger RCT, designed like the CAPRIT
study, with a longer follow-up may help to define the target Hb level.
Studies of treatment with iron in transplant recipients are scarce.
A small RCT (104 patients) comparing oral versus a single dose of IV iron after transplantation did not show a difference in time to anemia correction above 11 g/dL.
A meta-analysis showed the safety of IV iron for all indications; so it seems reasonable to treat transplanted patients
with IV iron.
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What is the level of evidence provided by this article?
Level V
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What is meant by the impact factor of a journal (please in your own words)?
Impact factor of a journal is a method by which to assess the importance of that journal. The higher is the impact factor of a journal, the more it is cited to different articles (books, thesis, journals etc); it has nothing to do with the quality of the contents of that journal. Also the journal should have completed at last 3 years from its first publication to be eligible for being assessed by impact factor.