Post-transplant Anemia Research Articles

Posttransplant Anemia as a Prognostic Factor of Mortality in Kidney-Transplant Recipients.

Background. Findings on the association between posttransplant anemia (PTA) and mortality in posttransplant patients are scarce. This study explored whether PTA shortly after kidney transplantation (KT) predicts mortality at up to 10 years' follow-up, stratified for chronic kidney disease (CKD) stages. Methods. PTA was divided into 3 categories according to the hemoglobin (Hb) value: severe (Hb < 10 g/dl), mild (10.0 g/dl ≤ Hb < 11.9 g/dl), or no PTA (Hb ≥ 12 g/dl). CKD stages were estimated using the CKD-EPI formula and divided into 2 groups: CKD1-2 and CKD3–5. Cox regression, stratified according to CKD, was performed to identify whether different categories of PTA predicted mortality in KT recipients. Results. Age, being female, and both mild and severe PTA contributed significantly to the Cox regression model on mortality in CKD1-2. In the Cox regression model for mortality in CKD3–5, age and severe PTA contributed significantly to this model. Conclusion. PTA shortly after KT increased the risk of mortality at up to 10 years' follow-up. Even mild PTA is associated with a 6-fold higher risk of mortality and severe PTA with a 10-fold higher risk of mortality in CKD1-2. Clinical evaluation and treatment of anemia might reduce the higher risk of mortality in patients with PTA in early stages of CKD after KT.

Spectrum of anemia after kidney transplantation: pathophysiology and therapeutic implications.

The prevalence of anemia in the first month after transplant is 70%-80%. The rate declines to 30%-40% at 3months and 20% by 12months. Its occurrence is influenced by the quality of the transplanted organ, bone marrow regenerative capacity, amount of surgical blood loss, and increased iron recycling. There is also a blunted response by oxidative inflammation to the effectiveness of supranormal levels of erythropoietin (EPO) release during ischemic-reperfusion allograft injury. The prevalence rate of late-onset post-transplant anemia (PTA) is 30%-50%. This category of patients falls into two ill-defined groups: (i) those with impaired renal capacity for EPO synthesis and (ii) those with bone marrow resistance. Given the difference in pathophysiology, the current KDIGO guideline that adopts uniform therapeutic approach for the two groups may be inappropriate. Comorbidity due to iron deficiency is common. Anemia is predictive of cardiovascular morbidity and shorter graft survival. Perhaps due to concern for the safe use of EPO stimulating agent (ESA) to correct anemia, there is often inadequate treatment of late-onset PTA. However, universal application of ESA may be harmful. Therefore, clinical trials are needed to define parameters for selecting patients (e.g., EPO assay) that will benefit the most from therapy for anemia.

Clinical risk factors associated with the post-transplant anemia in kidney transplant patients

BackgroundAnemia is a very common occurrence in post-renal transplant patients. Post-transplantation anemia (PTA) is associated with significant graft loss or cardiovascular morbidity. The objective of this study is to identify clinical risk factors associated with anemia after kidney transplantation. MethodsOur retrospective cohort study included a total of 570 renal transplant recipients. For the definition of anemia, we adopted “the lower limit of normal for Hgb concentration of blood” proposed by Beutler E and Waalen J [14], which has adjustments for age, gender and ethnicity. Post-transplant anemia (PTA) was defined as anemia that arose between 30 and 180days after transplantation. Based on this definition, of the 570 renal transplant recipients, 344 patients (62.1%) experienced PTA. The patients were divided into anemic and non-anemic groups, and a total of 20 clinical factors were compared between the two groups. ResultsIn the univariate analysis, age, race, multiple transplants, delayed graft function (DGF), and use of tacrolimus, sirolimus, thymoglobulin, ganciclovir, ACE inhibitors, and ARBs were associated with PTA. In the multivariate analysis, age (>60years old, OR=2.62, p=0.001), race (OR=2.54, p=0.001), and use of sirolimus (OR=2.01, p=0.019), antiviral agents (OR=1.96, p=0.015), thymoglobulin (OR=1.86, p=0.011), and DGF (OR=2.78, p=0.001) remained significant. ConclusionThe current results show that undergoing a transplant at age 60 or older, use of sirolimus, antiviral agents, and thymoglobulin are independent clinical risk factors associated with PTA. In terms of ethnicity, AA, MEA, or PI is higher risk for PTA and Hispanic is significantly lower risk for PTA compared to Caucasians.

Post renal transplant pure red cell aplasia-is tacrolimus a culprit?

Anemia is not uncommon in the post-renal transplant period and has been reported in up to 40% of renal transplant recipients. It is commonly due to drugs and infections. While post-transplantation anemia is usually due to graft dysfunction and drugs such as mycophenolate and cotrimoxazole, tacrolimus is an uncommon cause. Tacrolimus is usually not believed to be significantly myelosuppressive, but it can cause anemia due to thrombotic microangiopathy. A literature review shows a very small number of reported cases of pure red cell aplasia (PRCA) where tacrolimus seemed to be a causative agent. We report a case series of three renal transplant recipients who were on tacrolimus and presented with chronic transfusion requiring anemia due to PRCA.

Post-Transplant Anemia Has Strong Influences on Renal and Patient Outcomes in Living Kidney Transplant Patients

BackgroundPost-transplant anemia (PTA) is a risk factor for mortality and graft loss in kidney transplant patients. MethodsIn all, 172 patients were included in this study. PTA was defined as hemoglobin <13.0 g/dL in men and 12.0 g/dL in women. The primary outcome of interest was the renal outcome, defined as a 50% increase in serum levels of creatinine, a return to chronic dialysis, and subsequent kidney transplantation (KTx). The secondary outcome was a composite of the primary outcome and death. ResultsAt baseline, 75 patients (43.6%) had PTA. During follow-up of a median of 7.3 years, 52 patients (30.2%) had 2-fold higher creatinine levels than at baseline, 24 patients (14.0%) had to return to chronic dialysis or subsequent KTx, and 11 patients (6.4%) died; 8 (4.7%) of the deceased patients had functioning allografts. Univariate regression analyses showed that a lower hemoglobin level and positive proteinuria were significantly associated with both outcomes. After adjusting for important clinical variables, a lower hemoglobin level remained a strong predictor for both outcomes. Restricted cubic splines showed an almost linear inverse association with a hemoglobin level ≥12 g/dL. The risk of the outcomes increased with decreasing tertiles of the baseline hemoglobin level for both men and women, but the associations in women were much weaker than those in men, suggesting a different prognostic value of the hemoglobin level between men and women. ConclusionsPTA strongly influenced the renal and patient outcomes in living kidney transplant patients.

Laboratory use of hepcidin in renal transplant recipients.

Hepcidin is a small peptide with a critical role in cellular iron homeostasis, as it regulates utilization of stored iron and antimicrobial defense in inflammation (bacterial and fungal). Since it was isolated in 2000, and especially in the last decade, numerous studies aimed to evaluate the clinical use of plasma and urine hepcidin as a marker of anemia, especially anemia of chronic disease and post-transplant anemia (PTA). Hepcidin regulation is delicately tuned by two inflammatory pathways activated by interleukin-6 (IL-6) and bone morphogenic proteins (BMPs) and iron regulated pathway sensitive to circulating transferin-iron (TR-Fe) complex. BMP-mediated pathway and TR-Fe sensitive pathway seem to be connected by hemojuveline, a BMP co-factor that interacts with transferine receptor 2 (TRF2) in cases of high TR-Fe circulatory concentration. In addition to these regulatory mechanisms other regulators and signaling pathways are being extensively researched. Hepcidin has been identified as an important contributor to morbidity and mortality in end stage renal disease (ESRD) but no such association has jet been found in case of PTA. However, there is an association between higher doses of erythropoiesis-stimulating agents (ESA) and mortality in the posttransplant period and the assumption that hepcidin might play a role in ESA resistance in PTA. Thus the review’s main goal was to summarize papers published on the association of hepcidin with PTA, give up-to-date information on hepcidin regulation and on potential therapeutics that optimize hepcidin regulation. We also compared the performances of tests for hepcidin determination and reviewed research on immunosuppressants’ (IS) effect on hepcidin concentration.

Treatment With Darbepoetin During the First Year After Renal Transplantation: The Starting Point

IntroductionMultiple factors are associated with post-transplantation anemia, and renal function is the main factor. The aims of this study were to compare the evolution of hemoglobin in the first year post-transplantation according to darbepoetin (DA) treatment, and factors related to it, to evaluate the difference between earlier versus delayed treatment, and to describe the dose change pattern. Patients and MethodsWe describe a retrospective study of cohorts in 462 transplant recipients (2004–2011). The variables reported were from donor, transplantation recipient, and DA treatment. ResultsIn this study, 67.5% of patients were treated with DA, 32.5% were not. The comparison of hemoglobin in both groups during the first year showed a similar evolution with significant differences between consecutive measures until the second trimester. The hemoglobin of the treated group was significantly lower. The evolution of renal function was not different. Multivariate analysis related DA treatment to delayed graft function (DGF) and albuminuria in the first year. Patients with early versus delayed DA introduction did not show a difference regarding length of treatment, but the total dose in the delayed introduction was lower. The evolution of creatinine and hemoglobin was similar in both groups. ConclusionThe introduction of DA was related to DGF and albuminuria. The delayed introduction of DA meant the following: less total dose than earlier introduction, no difference in length of treatment, and a similar evolution in hemoglobin and renal function in both groups. The lack of guidelines about DA treatment in renal transplantation makes it difficult to establish a pattern of dose adjustment.

Post-renal transplantation anemia at 12 months: prevalence, risk factors, and impact on clinical outcomes.

To investigate any association between post-transplantation anemia (PTA) and clinical outcomes following living donor kidney transplantation. We retrospectively evaluated 887 patients who received living donor kidney transplantations at our medical center between January 2006 and December 2012 to evaluate whether PTA, defined as serum hemoglobin (Hb) levels of <130 g/l in men and <120 g/l in women, at 12 months is associated with post-transplant outcomes, including graft function, death-censored graft survival, or patient survival. The prevalence of PTA at 1, 3, 6, and 12 months was 84.3, 39.5, 26.2, and 21.6 %, respectively. Donor age [hazard ratio (HR), 1.03; 95 % confidence interval (CI) 1.01-1.05] and acute rejection (HR 2.13; 95 % CI 1.28-3.54) were found to be independent risk factors for PTA at 12 months. Recipient age (HR 0.98; 95 % CI 0.95-1.00), pre-transplantation Hb levels (HR 0.99; 95 % CI 0.98-1.00), and estimated glomerular filtration rates (eGFRs) at 12 months (HR 0.96; 95 % CI 0.94-0.97) were found to confer slight protection against PTA at 12 months. PTA at 12 months was associated with increased graft loss (HR 1.046; 95 % CI 1.045-1.046). For each increase in anemia degree, there was a 2.77-fold greater risk of graft loss (HR 2.77; 95 % CI 1.50-5.13). When stratified according to eGFR, PTA was found to be a predictor of graft loss in patients with an eGFR of <60 ml/min/1.73 m(2) (HR 4.57; 95 % CI 1.98-10.56) but not in patients with an eGFR of >60 ml/min/1.73 m(2) (HR 1.89; 95 % CI 0.13-27.78). PTA was not found to be a predictor of patient survival. Anemia is common after kidney transplantation, and its prevalence declines with time after transplantation. Presence of anemia at 12 months post-transplant was an independent predictor of graft loss, with higher risk of graft loss in patients with anemia and poorer kidney functions.

Pre-Transplant Erythropoiesis-Stimulating Agent Hypo-Responsiveness and Post-Transplant Anemia

BackgroundAt the time of kidney transplantation (KT), almost all patients have anemia caused by low levels of endogenous erythropoietin (EPO), along with several other factors. After KT, anemia improves because of secretion of EPO from the allograft. But some recipients have persistent anemia. Whether or not erythropoiesis-stimulating agent (ESA) hypo-responsiveness before KT affects post-transplant anemia (PTA) remains unknown. MethodsSixty-eight patients received KT between January 2007 and July 2012 through the Department of Urology at Kobe University Hospital, and 35 of these patients were enrolled. Exclusion criteria included age <18 years, unknown ESA dosage at transplantation, ESA start within 1 year after transplantation, and other criteria. We evaluated post-transplant hemoglobin (Hb) levels from the pre-transplant ESA responsive index (ERI): pre-transplant ESA dosage/Hb × body weight at 1 year after transplantation. ResultsThe mean (±SD) Hb of all patients rose from 11.3 ± 1.0 mg/dL to 12.7 ± 1.4 mg/dL at 1 year after transplantation (P < .01). The pre-transplant low ERI group (<10) showed significantly higher hemoglobin levels compared with the pre-transplant high ERI group (≥10; 12.9 ± 1.14 mg/dL versus 11.8 ± 1.76 mg/dL, respectively; P = .03). ConclusionsESA hypo-responsiveness before KT carried over after KT. Low pre-transplant ERI might be a sentinel marker for PTA.

Post-transplantation Anemia Predicts Cardiovascular Morbidity and Poor Graft Function in Kidney Transplant Recipients

ObjectiveWe aimed to investigate whether low post-transplantation-period hemoglobin levels are predictive of cardiovascular morbidity in terms of left ventricular (LV) hypertrophy and vascular stiffness and to determine the contributing factors of post-transplantation anemia in kidney transplant (KT) recipients. MethodsOne hundred fifty (mean age, 38.9 ± 10.8 y; 113 male) KT recipients with functioning grafts were enrolled in the study. All subjects underwent clinical and laboratory evaluations (24-hour urinary protein loss, complete blood count) and transthoracic echocardiography to assess LV systolic function. Arterial stiffness was measured by means of carotid-femoral pulse-wave velocity (PWV). Mean hemoglobin levels were analyzed at the 1st, 6th, 12th, and 24th months after transplantation. Patients were divided into 2 groups according to presence of anemia: patients with anemia (group 1; n = 120) and normal (group 2; n = 30). ResultsPWV values (6.8 ± 1.9 m/s vs 6.4 ± 1.1 m/s in groups 1 and 2, respectively; P = .002) and LV mass index (LVMI; 252.1 ± 93.7 g/m2 vs 161.2 ± 38.5 g/m2 groups 1 and 2, respectively; P = .001) were significantly higher in group 1. Estimated glomerular filtration rate and (64 ± 28.5 m/min vs 77.8 ± 30 m/min in groups 1 and 2, respectively; P = .001) LV systolic function (57.2 ± 5.8% vs 77.8 ± 30% in groups 1 and 2, respectively; P < .005) were significantly lower in group 1. In regression analysis, LV systolic function and LVMI were predictors of post-transplantation hemoglobin levels. ConclusionsPost-transplantation anemia contributes to cardiovascular morbidity by deteriorating LV function and increasing PWV and is therefore associated with poor prognosis for graft survival. Early correction of post-transplantation anemia, especially with the use of erythropoietin, may be beneficial for both graft and recipient survivals.

Passenger lymphocyte syndrome in ABO and Rhesus D minor mismatched liver and kidney transplantation: A prospective analysis

The increasing demand for solid organs has necessitated the use of ABO and Rhesus (Rh) D minor mismatched transplants. The passenger lymphocyte syndrome (PLS) occurs when donor lymphocytes produce antibodies that react with host red blood cell (RBC) antigens and result in hemolysis. Our aim was to evaluate prospectively the role of PLS in post transplant anemia and hemolysis in ABO and RhD minor mismatched recipients of liver and kidney grafts and to study the association of PLS with donor lymphocyte microchimerism. We examined 11 liver and 10 kidney recipients at Day +15 for anemia, markers of hemolysis, direct antiglobulin test and eluates, and serum RBC antibodies. Microchimerism was determined in peripheral blood lymphocytes by genotyping of simple sequence length polymorphisms encoding short tandem repeats. Immune hemolytic anemia and anti-recipient RBC antibodies were observed in 2 out of 11 liver (18.2%) and 2 out of 10 kidney (20%) transplants. RBC antibody specificity reflected the donor to recipient transplant, with anti-blood group B antibodies identified in 2 cases of O to B and 1 case of A to AB transplants while anti-D antibodies were detected in 1 case of RhD-negative to RhD-positive transplant. Donor microchimerism was found in only 1 patient. In conclusion, passenger lymphocyte mediated hemolysis is frequent in minor mismatched liver and kidney transplantation. Recognizing PLS as a potential cause of post transplant anemia may allow for early diagnosis and management to decrease the morbidity and mortality in some patients.

Blood disorders typically associated with renal transplantation.

Renal transplantation has become one of the most common surgical procedures performed to replace a diseased kidney with a healthy kidney from a donor. It can help patients with kidney failure live decades longer. However, renal transplantation also faces a risk of developing various blood disorders. The blood disorders typically associated with renal transplantation can be divided into two main categories: (1) Common disorders including post-transplant anemia (PTA), post-transplant lymphoproliferative disorder (PTLD), post-transplant erythrocytosis (PTE), and post-transplant cytopenias (PTC, leukopenia/neutropenia, thrombocytopenia, and pancytopenia); and (2) Uncommon but serious disorders including hemophagocytic syndrome (HPS), thrombotic microangiopathy (TMA), therapy-related myelodysplasia (t-MDS), and therapy-related acute myeloid leukemia (t-AML). Although many etiological factors involve the development of post-transplant blood disorders, immunosuppressive agents, and viral infections could be the two major contributors to most blood disorders and cause hematological abnormalities and immunodeficiency by suppressing hematopoietic function of bone marrow. Hematological abnormalities and immunodeficiency will result in severe clinical outcomes in renal transplant recipients. Understanding how blood disorders develop will help cure these life-threatening complications. A potential therapeutic strategy against post-transplant blood disorders should focus on tapering immunosuppression or replacing myelotoxic immunosuppressive drugs with lower toxic alternatives, recognizing and treating promptly the etiological virus, bacteria, or protozoan, restoring both hematopoietic function of bone marrow and normal blood counts, and improving kidney graft survival.

Influence of Anemia on Patient and Graft Survival After Renal Transplantation

Contradictory results are reported concerning the influence of anemia on patient and graft survival after renal transplantation. Assuming that level of renal function and anemia are strongly correlated, posttransplantation anemia (PTA) may have a different impact depending on the stage of chronic kidney disease (CKD). This study is a retrospective multicenter analysis using the DIVAT French database. The prevalence, risk factors, and influence of 12-month PTA (World Health Organization's definition) on patient and graft survival were analyzed according to CKD stage (Modification of Diet in Renal Disease equation). The prevalence of 12-month PTA in our cohort of 4217 patients was 41.1%. Multivariate analysis demonstrated that worse renal function, donor age, period of transplantation, induction therapy, and mTOR inhibitors were significant risk factors for PTA. Posttransplantation anemia was a significant risk factor for all-cause mortality in CKD stages 1 to 2T (hazard ratio, 2.39; 95% confidence interval, 1.99-4.40) and 3T (hazard ratio, 1.52; 95% confidence interval, 1.08-2.15) and for cardiovascular mortality only on CKD stages 1T and 2T. In renal transplant recipients with CKD stages 4 to 5T, patient and graft survival were similar in patients with versus without anemia. Graft survival was not influenced by PTA, whatever the CKD stage. Posttransplantation anemia is associated with decreased patient survival only in CKD stages 1T, 2T, and 3T. Posttransplantation anemia has no influence on graft survival regardless of CKD stage.

Prevalence and management of post-transplant anemia in long-term follow-up of Chinese kidney transplant recipients: a single-center report

BackgroundPost-transplant anemia (PTA) has long been a less-recognized complication in kidney transplant recipients, and its prevalence also tends to be underestimated. This study sought to evaluate the prevalence, management, and risk factors of PTA from a group of long-term follow-up Chinese kidney transplant recipients.MethodsOne hundred and fifty-four adult kidney transplant recipients were followed up at Fuzhou General Hospital, China, and retrospectively studied.ResultsPTA prevalence at transplant and at 5-yearly time points after transplantation were 45.5%, 10.7%, 9.6%, 14.8%, 13.5%, and 19.6%, respectively. Overall, 38.3% of patients had been anemic at least once during the follow-up period, and 42% of these patients had recurrent anemia. Correlation analysis indicated that hemoglobin levels were associated with graft function. No correlations between anemia and age, gender, immunosuppressive regimens, or antihypertensive agents were observed. Binary logistic regression analysis suggested that serum creatinine and blood urea nitrogen were associated with the diagnosis of anemia at 1 year post-transplant. At 5 years post-transplant, only serum creatinine concentrations correlated with anemia. Although iron drugs are frequently used, erythropoietin was rarely administered in those anemic patients suffering poor graft function that necessitated such therapies.ConclusionsThe prevalence of PTA is noticeably high, and impaired kidney graft function seemed to be the major risk factor for anemia. There is an urgent need to improve current PTA management and to establish modified guidelines for this common complication in kidney transplant recipients.

Blood disorders after kidney transplantation

Post transplant anemia (PTA) is a common issue in kidney transplant recipients. Most importantly it is associated with an impaired allograft function. Other important factors associated with PTA are immunosuppressive drugs (MPA, AZA and SRL), iron deficiency, infections (Parvo B19), older donor age, rejection episodes, an increased inflammatory state, and erythropoietin hyporesponsiveness. As there are no adequately powered RCTs in the kidney transplant population on anemia treatment with ESA, we have to rely on what we know from the large RCTs in the CKD population. The recently published KDIGO guidelines do not recommend treatment with ESA if Hb is >10 g/dl. Repletion of iron stores is emphasized. Post transplant leukopenia (PTL) and thrombocytopenia (PTT) are frequent complications especially in the first six months after kidney transplantation. Myelosuppression caused by immunosuppressive agents (MPA, AZA, SRL, rATG), antimicrobial drugs (VGCV), and CMV infection is the predominant cause. There are no widely accepted guidelines on treatment strategies, but most often dose reduction or discontinuation of causative medication is done. Most clinicians tend to decrease MPA dose, but this is eventually associated with an increase in acute rejection episodes. VGCV dose reduction (preemptive treatment instead of CMV prophylaxis) may be a successful strategy. In severe cases G-CSF treatment is an important management option and seems to be safe.

Renal Interstitial Fibrosis in 0-Hour Biopsy as a Predictor of Post-Transplant Anemia

Background/Aims: Anemia is common in kidney transplant patients and may cause adverse cardiovascular events. Several studies have reported some predictors of post-transplant anemia. However, associations between the pathological findings in the 0-hour biopsy and anemia have not been well described. Methods: 258 consecutive kidney transplant patients were enrolled in this retrospective study. The patients were divided into two groups, according to the presence or absence of interstitial fibrosis and tubular atrophy (IF/TA) in the 0-hour biopsy: the IF/TA group with fibrotic area ≥5% (n = 131) and the non-IF/TA group with fibrotic area <5% (n = 127). We examined the association between IF/TA and post-transplant anemia. Results: Serial changes in hemoglobin levels in the IF/TA group were lower than in the non-IF/TA group (p = 0.007). Anemia at 12 months was found in 53% of the IF/TA group, and 35% of the non-IF/TA group (p = 0.004). Even after adjustment for several confounders including graft function, the presence of IF/TA was independently associated with post-transplant anemia at 12 months (odds ratio 1.88, 95% confidence interval 1.06-3.36, p = 0.031). This association was still significant in a subgroup with normal graft function. Conclusions: IF/TA in the 0-hour biopsy specimen is one of the predictors for post-transplant anemia and can be used to identify patients who need the treatment with erythropoiesis-stimulating agents.

Anemia is a predictor of graft loss but not cardiovascular events and all‐cause mortality in renal transplant recipients: follow‐up data from the ALERT study

It is well established that post-transplantation anemia (PTA) in renal transplant recipients (RTRs) is associated with reduced graft survival. However, there is an uncertainty of the effect of PTA on cardiovascular events and all-cause mortality. We examined prospectively in a large cohort of erythropoietin-naive patients the effects of PTA on cardiovascular morbidity, patient survival, and graft survival. A prospective cohort study of RTRs (n = 2102) included in the ALERT study. Cox regression models were used to evaluate the impact of PTA on study endpoints: first occurrence of a major adverse cardiac event, all-cause death, and the incidence of death-censored graft loss. Mean follow-up was 6.7 yr. All endpoints were adjudicated by an independent endpoint committee. Twenty-nine percent of women and 30% of men were anemic. Hemoglobin levels were not associated with any effect on cardiovascular morbidity and mortality (HR 0.97 [0.90-1.05] per g/dL, p = 0.48) or all-cause death (HR 0.96 [0.90-1.03] per g/dL, p = 0.24) after extensive multivariate adjustments for clinical and demographic factors. Hemoglobin levels were negatively associated with graft loss (HR 0.86 [0.80-0.92] per g/dL, p < 0.001). PTA was not associated with an increased incidence of cardiovascular morbidity and mortality or all-cause mortality.

Anemia in Living Donor Kidney Transplantation

BackgroundWe evaluated the prevalence of pretransplantation and posttransplantation anemia and its effect on serum creatinine levels among living donor kidney transplant recipients. MethodsWe reviewed retrospectively 170 adult patients who underwent living donor kidney transplantation between 1994 and 2009. We defined anemia as hemoglobin (Hb) ≤12 g/dL for women and ≤13 g/dL for men with severe anemia as Hb <11 g/dL for both men and women (World Health Organization criteria). Patients were also categorized according to Hb levels less than or greater than 10 g/dL for correlation with recipient serum creatinine levels at months 1, 3, 6, and 12. ResultsMean recipient and donor ages were 33 ± 10 and 45 ± 12 years, respectively. Mean cold ischemia time was 76 ± 43 minutes. At the time of transplantation, anemia and severe anemia prevalences were 86.7% and 58.8%, respectively. Anemia was observed in 64 patients (42.1%) at posttransplantation month 3. Pretransplantation severe anemia was a good predictor of both Hb levels and anemia presence posttransplantation. Pretransplantation anemia and severe anemia caused greater requirements for posttransplantation blood transfusions (P < .05). Younger age and female gender were significant risk factors for severe anemia pretransplantation. There was a significant correlation between posttransplantation Hb levels and serum creatinine levels at 12 month (P = .01). Recipient female gender and longer hospital stay were significant risk factors for both anemia and severe anemia posttransplantation. Higher recipient weight and history of acute rejection episode were also significant for posttransplantation severe anemia. ConclusionThis study indicated that successful kidney transplantation had a positive effect on Hb levels. Posttransplantation anemia predicted worse graft function in the first month after transplantation.

The Impact of Post-transplant Hemoglobin Level on Renal Allograft Outcome

BackgroundAnemia is a common complication of chronic renal disease and renal transplantation. Early post-transplant anemia is the consequence of blood loss, immunosuppressant therapy, and failure to produce sufficient erythropoietin. Late post-transplant anemia has been attributed to drug therapy, renal dysfunction, and infection. The effect of post-transplant anemia on renal allograft survival and acute rejection rates is not established. The aim of this study was to examine the impact of post-transplant anemia on renal function and allograft outcomes. Materials and methodsWe included 411 patients who underwent living or deceased donor renal transplantations in our center from April 1990 to March 2010. The patients were divided into 2 groups according to their postoperative hemoglobin level at 1 month: anemic group (<12.0 g/dL in men, <11.0 g/dL in women) and nonanemic group (≥12.0 g/dL in men, ≥11.0 g/dL in wemen). The outcome measures included postoperative serum creatinine levels at 12 and 36 months, acute and chronic rejection rates, as well as long-term graft survival. ResultsThe acute and chronic rejection rates were significantly higher in the anemic group: 28.1% versus 19.7% (P = .000) and 24.1% versus 19.7% (P = .027), respectively. Postoperative serum creatinine levels at 12 and 36 months were not significantly different in patients with functioning grafts regardless of their anemia status (P = .530 and P = .430, respectively). Graft survival was lower with anemia: 85.4% versus 93.8% at 5 years, and 74.8% versus 83.5% at 10 years (P = .040). ConclusionsPost-transplant anemia was associated with poorer renal function at 12 months, higher acute rejection rates, and worse long-term renal allograft outcomes compared with subjects displaying normal hemoglobin levels.

Clinical profile and post-transplant anaemia in renal transplant recipients restarting dialysis after a failed graft: changing trends between 2001 and 2009.

BackgroundThe aim of this study was to compare the clinical profile, outcome and the prevalence and management of anaemia between two cohorts of renal transplant patients with graft failure restarting dialysis in 2001 and 2009.MethodsCross-sectional, observational, retrospective and multicentre study of 397 patients in the 2001 cohort and 222 in the 2009 cohort. Data were recorded at 0, 3, 6, 9 and 12 months before the onset of dialysis resumption and during the first 90 days after restarting dialysis (mortality and hospital admission).ResultsPatients in the 2009 cohort were older at the time of inclusion in the study and transplantation, and restarted dialysis therapy with a significantly better glomerular filtration rate. In both cohorts, there was a rapid deterioration of renal function with statistically significant differences in serum creatinine and glomerular filtration rate between the monthly intervals −12 and 0. The mean haemoglobin value at −12 months was 11.6 g/dL [7.2 mmol/L] in the 2001 cohort when compared with 12.3 g/dL [7.6 mmol/L] in the 2009 cohort, and at the time of restarting dialysis 9.6 g/dL [6.0 mmol/L] versus 10.6 g/dL [6.6 mmol/L]. The percentage of patients treated with erythropoiesis-stimulating agents, at any time during the 12 months before readmission to dialysis, increased significantly from 61.5% in the 2001 cohort to 96% in the 2009 cohort. There were no significant differences between the 2001 and 2009 cohorts in mortality rate (8.8 versus 9.0%) or hospital admission (31.5 versus 31.1%) during the study time.ConclusionsAt restarting dialysis, the proportion of patients with anaemia (and its severity) due to progressive graft nephropathy decreased over the past 8 years, increasing significantly the percentage of patients treated with erythropoietin. Differences in morbimortality after dialysis resumption were not observed, this is probably due to an increase in the age of donors and recipients.