FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2078993832> ?p ?o ?g. }

• W2078993832 endingPage "536" @default.
• W2078993832 startingPage "519" @default.
• W2078993832 abstract "Anemia in the setting of chronic kidney disease is a well-recognized phenomenon that is associated with decreasing renal function and deficiency of or resistance to erythropoietin. However, anemia in the post–renal transplantation setting has received comparatively less attention in the literature. In this review, we aim critically to appraise the available literature regarding posttransplantation anemia, concentrating in particular on the prevalence of posttransplantation anemia, its etiopathogenesis, potential effects on morbidity and mortality, and the rationale for intervention and treatment. Despite deficiencies in the literature, we conclude that posttransplantation anemia is a common phenomenon that can occur either early or late posttransplantation, and its causation is usually multifactorial and includes contributions notably from poor or decreasing renal function, immunosuppression, and iron deficiency. Conversely, there is a shortage of well-conducted prospective studies looking at the morbidity attributable to posttransplantation anemia and a lack of trial evidence to determine whether intervention improves patient morbidity and outcome. Anemia in the setting of chronic kidney disease is a well-recognized phenomenon that is associated with decreasing renal function and deficiency of or resistance to erythropoietin. However, anemia in the post–renal transplantation setting has received comparatively less attention in the literature. In this review, we aim critically to appraise the available literature regarding posttransplantation anemia, concentrating in particular on the prevalence of posttransplantation anemia, its etiopathogenesis, potential effects on morbidity and mortality, and the rationale for intervention and treatment. Despite deficiencies in the literature, we conclude that posttransplantation anemia is a common phenomenon that can occur either early or late posttransplantation, and its causation is usually multifactorial and includes contributions notably from poor or decreasing renal function, immunosuppression, and iron deficiency. Conversely, there is a shortage of well-conducted prospective studies looking at the morbidity attributable to posttransplantation anemia and a lack of trial evidence to determine whether intervention improves patient morbidity and outcome. THE KIDNEY DISEASE OUTCOMES Quality Initiative (KDOQI) classified chronic kidney disease (CKD) into stages 1 to 5 based on estimated glomerular filtration rate (eGFR). CKD stage 1 is defined as normal GFR (>90 mL/min [>1.5 mL/s]) with urine findings, structural abnormality, or a genetic trait pointing to kidney disease. CKD stages 2, 3, 4, and 5 are defined on the basis of decreasing GFR (69 to 89, 30 to 59, 15 to 29, and <15 mL/min [1 to 1.48, 0.5 to 0.98, 0.25 to 0.48, and <0.25 mL/s], respectively). Anemia in the context of CKD is a well-recognized phenomenon associated with worsening renal function.1Eschbach J.W. Adamson J.W. Anemia of end-stage renal disease (ESRD).Kidney Int. 1985; 28: 1-5Crossref PubMed Scopus (287) Google Scholar The presence of anemia contributes to many of the symptoms concomitant with uremia, and its treatment is a central part of the management of patients with CKD.2Silverberg D.S. Wexler D. Blum B. et al.Anemia in chronic kidney disease and congestive heart failure.Blood Purif. 2003; 21: 124-130Crossref PubMed Scopus (19) Google Scholar, 3Snyder J.J. Foley R.N. Gilbertson D.T. et al.Hemoglobin levels and erythropoietin doses in hemodialysis and peritoneal dialysis patients in the United States.J Am Soc Nephrol. 2004; 15: 174-179Crossref PubMed Scopus (43) Google Scholar, 4Macdougall I.C. Erythropoietin and renal failure.Curr Hematol Rep. 2003; 2: 459-464PubMed Google Scholar Anemia in this setting usually is a result of erythropoietin (EPO) deficiency, resistance to EPO, iron deficiency (either absolute or functional), and/or blood loss. The development and persistence of anemia in patients with CKD is associated with poorer quality of life; decreased exercise tolerance, mental agility, and renal and cardiac function; increased hospitalization; and decreased survival on dialysis therapy.5Roger S.D. McMahon L.P. Clarkson A. et al.Effects of early and late intervention with epoetin alpha on left ventricular mass among patients with chronic kidney disease (stage 3 or 4): Results of a randomized clinical trial.J Am Soc Nephrol. 2004; 15: 148-156Crossref PubMed Scopus (198) Google Scholar, 6Locatelli F. Pisoni R.L. Combe C. et al.Anemia in hemodialysis patients of five European countries: Association with morbidity and mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS).Nephrol Dial Transplant. 2004; 19: 121-132Crossref PubMed Scopus (375) Google Scholar, 7Gouva C. Nikolopoulos P. Ioannidis J.P. et al.Treating anemia early in renal failure patients slows the decline of renal function: A randomized controlled trial.Kidney Int. 2004; 66: 753-760Crossref PubMed Scopus (367) Google Scholar Consequently, since the advent of erythropoiesis-stimulating agents and parenteral iron formulations, by the time patients start renal replacement therapy, the use of iron supplementation8Afzali B. Goldsmith D.J. Intravenous iron therapy in renal failure: Friend and foe?.J Nephrol. 2004; 17: 487-495PubMed Google Scholar coupled with erythropoiesis-stimulating agents is very common.6Locatelli F. Pisoni R.L. Combe C. et al.Anemia in hemodialysis patients of five European countries: Association with morbidity and mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS).Nephrol Dial Transplant. 2004; 19: 121-132Crossref PubMed Scopus (375) Google Scholar Nevertheless, despite demonstrable benefits derived from correcting anemia9Evans R.W. Rader B. Manninen D.L. Cooperative Multicenter EPO Clinical Trial Group: The quality of life of hemodialysis recipients treated with recombinant human erythropoietin.JAMA. 1990; 263: 825-830Crossref PubMed Scopus (402) Google Scholar, 10Grutzmacher P. Scheurmann E. Low I. et al.Correction of renal anemia by recombinant human erythropoietin: Effects on myocardial function.Contrib Nephrol. 1988; 66: 176-184PubMed Google Scholar, 11Delano B.G. Improvements in quality of life following treatment with r-HuEPO in anemic hemodialysis patients.Am J Kidney Dis. 1989; 14: 14-18PubMed Google Scholar, 12Consensus Development Conference PanelMorbidity and mortality of renal dialysis: An NIH consensus conference statement.Ann Intern Med. 1994; 121: 62-70Crossref PubMed Scopus (236) Google Scholar and the advocacy of widely available and respected best practice guidelines,6Locatelli F. Pisoni R.L. Combe C. et al.Anemia in hemodialysis patients of five European countries: Association with morbidity and mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS).Nephrol Dial Transplant. 2004; 19: 121-132Crossref PubMed Scopus (375) Google Scholar the prevalence of anemia in dialysis patients is not as low as one would expect. This phenomenon can be explained in part by the cost of erythropoiesis-stimulating agents, delayed start of therapy (eg, through late recognition of CKD), and resistance to erythropoiesis-stimulating agents (eg, hyperparathyroidism, hematinic deficiency, and chronic inflammation). The development of anemia in the setting of renal transplantation (posttransplantation anemia), in contrast to that in the CKD and dialysis populations, has received far less attention in the literature. Before the widespread use of erythropoiesis-stimulating agents, most renal transplant recipients were anemic in the early postengraftment period because of preexisting anemia exacerbated by perioperative blood loss. With restoration of endogenous EPO secretion by the allograft, which occurs hours after successful engraftment, there was at least partial correction of anemia during the next 6 months. However, posttransplantation anemia has not disappeared after widespread use of erythropoiesis-stimulating agents. To some extent, this issue has been “overlooked” by the transplant community (as, it also may be argued, have been other sequelae of transplantation, such as dyslipidemia and hypertension), whose focus historically has been prevention of rejection and achievement of good renal function. However, continuing improvements in 1-year allograft and patient survival rates and allograft “half-life” have brought about a shift in emphasis, with greater importance on control of various cardiovascular risk factors relevant to survival of renal transplant recipients.13Magee C.C. Pascual M. Update in renal transplantation.Arch Intern Med. 2004; 164: 1373-1388Crossref PubMed Scopus (91) Google Scholar This new emphasis is supported strongly by the fact that the most common cause of allograft loss is death (mostly cardiovascular) of patients with functioning allografts, and also the realization that “cardiovascular” risk factors are very relevant to the second most common cause of allograft loss, chronic allograft nephropathy (CAN).14Offermann G. Immunosuppression for long-term maintenance of renal allograft function.Drugs. 2004; 64: 1325-1338Crossref PubMed Scopus (38) Google Scholar The purpose of this review is critically to appraise the literature regarding posttransplantation anemia by using recently published reports to focus on causation, potential morbidity, and the rationale for intervention to correct anemia in this clinical context. For this purpose, a thorough search of PubMed was conducted, and all relevant articles were obtained and read. Before discussing prevalence, it is necessary to state the obvious; the prevalence of anemia depends critically on its definition. It is surprisingly diverse in the literature. The World Health Organization (WHO) defines anemia as a hemoglobin level less than 13 g/dL (<130 g/L) in men and less than 12 g/dL (<120 g/L) in women (ie, any hemoglobin values less than sex-determined normal ranges, irrespective of age and menopausal status).15WHO: Nutritional AnemiaWorld Health Organization Technical Report Series No. 405. World Health Organization, Geneva, Switzerland1968Google Scholar This definition is disparate to the KDOQI16National Kidney FoundationK/DOQI Clinical Practice Guidelines for Anemia of Chronic Kidney Disease.Am J Kidney Dis. 2001; 37: S182-S238PubMed Google Scholar and United Kingdom Renal Association17The Renal AssociationTreatment of Adults and Children With Renal Failure. (ed 3). Royal College of Physicians of London and the Renal Association, London, UK2002Google Scholar criteria of hemoglobin level less than 12 g/dL (<120 g/L) in men and postmenopausal women and less than 11 g/dL (<11 g/L) in menstruating women. To add a layer of complexity, the Revised European Best Practice Guidelines define anemia as a hemoglobin level 2 SDs less than the population mean, ie, less than 11.5 g/dL (<115 g/L) in adult women, less than 13.5 g/dL (<135 g/L) in adult men, and less than 12.0 g/dL (<120 g/L) in adult men older than 70 years. With the evident heterogeneity in defining anemia, it is no surprise that there is great discrepancy in the literature with regard to the actual prevalence of posttransplantation anemia. In a sense, what you measure is how you measure it. One additional level of complexity that leads to disagreement between studies aimed at quantifying posttransplantation anemia is the time at which measurements of hemoglobin are obtained; as already mentioned, anemia in the period shortly after engraftment tends to be fairly universal (this concept of “early” [compared with “late”] posttransplantation anemia is elaborated on later). That is, what you measure is not only how you measure it, but also when you measure it. Nevertheless, a number of epidemiological studies attempted to quantify the prevalence of posttransplantation anemia (Table 1). Among these, the TRansplant European Study on Anemia Management (TRESAM) Study was a cross-sectional survey using a questionnaire-based analysis from 72 transplant centers in 16 countries involving 4,263 patients who had received a transplant 6 months or 1, 3, or 5 years earlier. Information was gathered in 2000 and 2001.18Vanrenterghem Y. Ponticelli C. Morales J.M. et al.Prevalence and management of anemia in renal transplant recipients: A European survey.Am J Transplant. 2003; 3: 835-845Crossref PubMed Scopus (262) Google Scholar Defining anemia as a hemoglobin level less than 13 g/dL (<130 g/L) for men and less than 12 g/dL (<120 g/L) for women, the investigators reported a prevalence of anemia of 38.6% at enrollment. Although 8.5% of subjects were severely anemic (defined as hemoglobin < 11 g/dL [<110 g/L] for men and <10 g/dL [<100 g/L] for women), only 17.8% were treated with an erythropoiesis-stimulating agent. Mean hemoglobin level in patients administered an erythropoiesis-stimulating agent was 11.1 ± 2.0 g/dL (111 ± 20 g/L) compared with patients not administered an erythropoiesis-stimulating agent (13.1 ± 2.1 g/dL [131 ± 21 g/L]; P < 0.05). Severely anemic patients administered EPO had a better (WHO) performance score than those not treated.18Vanrenterghem Y. Ponticelli C. Morales J.M. et al.Prevalence and management of anemia in renal transplant recipients: A European survey.Am J Transplant. 2003; 3: 835-845Crossref PubMed Scopus (262) Google Scholar, 19Vanrenterghem Y. Anemia after renal transplantation.Nephrol Dial Transplant. 2004; 19: SV54-SV58Google ScholarTable 1Prevalence and Predictors of Posttransplantation AnemiaAuthorPublicationNo. of PatientsMean Hemoglobin (g/dL)Summary of FindingsCommentaryVanrenterghem et alAm J Transplant 3:834-845, 20034,26313.2 ± 1.9 at 5 yCross-sectional survey; 38.6% anemia prevalence at enrollment; 9% with severe anemia. Strong negative association between hemoglobin level and poor graft function. Treatment with ACE inhibitors/ARBs, MMF, and AZA also associated with higher likelihood of anemia. Very low prevalence of erythropoiesis-stimulating agent use.TRESAM Study of prevalence of posttransplantation anemia; largest study of its kind; 5-y follow-up data; showed very low erythropoiesis-stimulating agent use despite high prevalence of anemia; lacking data pertaining to iron statusShibagaki et alNephrol Dial Transplant 19:2368-2373, 200419213.0 ± 0.1 at 1 y20% of patients had severe anemia at 6 mo and 1 y. Multivariate analysis showed serum creatinine as strong independent risk factor for anemia. African-American race was a risk factor at 6 mo, and female sex, at 1 y. Only 36% of anemic patients had iron indices checked in the first year posttransplantation.Single-center study, 1-y follow-up dataMix et alAm J Transplant 3:1426-1433, 2003240Mean hematocrit, 38% at 60 mo76%, 21%, and 36% prevalence of anemia (hematocrit < 36%) at transplantation and 1 and 4 y posttransplantation. Female sex was a risk factor, but diabetes was not. Only 36% had iron studies; 46% administered iron supplement, and 40%, erythropoiesis-stimulating agent.Retrospective cohort study with 4-y follow-up data; showed poor investigation and treatment of posttransplantation anemiaKausman et alPediatr Nephrol 19:526-530, 20045011.0 (range, 62-154)60% overall prevalence of anemia; 30% severe anemia. High prevalence of iron deficiency (34%). Tacrolimus therapy and serum creatinine were significant independent predictors of anemia. ACE inhibitors were not associated with anemia.Pediatric study; cross-sectional design; age-specific definitions of anemiaShah et alTransplantation 81:1112-1118, 20061,15112.9 ± 1.645% prevalence of anemia, but only 145 administered erythropoiesis-stimulating agents. Age, female sex, renal function, serum ferritin, and ACE-inhibitor therapy were independent predictors of anemia. Renal function was the greatest predictor of anemia.3 Centers; cross-sectional designKarthikeyan et alAm J Transplant 4:262-269, 200445914.2 ± 1.6 at stage 1 to 11.7 ± 1.1 at stage 5CKD present in 412 subjects. Prevalence of anemia increased from 0% in stage 1 to 33% in stage 5. Low ferritin (<100 ng/mL) in 50% of patients in CKD stages 3-5, but 0% in stage 1.Predominantly CKD study in transplantation; cross-sectional design; only 60% of patients with anemia had iron indices measuredNOTE. Hemoglobin expressed as mean ± SD unless otherwise stated. Key publications studying the prevalence and predictors of anemia after renal transplantation are presented. To convert hemoglobin in g/dL to g/L, multiply by 10. Open table in a new tab NOTE. Hemoglobin expressed as mean ± SD unless otherwise stated. Key publications studying the prevalence and predictors of anemia after renal transplantation are presented. To convert hemoglobin in g/dL to g/L, multiply by 10. Other studies also confirmed the high prevalence of anemia reported by TRESAM, although there are expected differences in the actual figures dependent on the definition of anemia used and the time observations were made. In a prospective study, Moore et al20Moore L.W. Smith S.O. Winsett R.P. et al.Factors affecting erythropoietin production and correction of anemia in kidney transplant recipients.Clin Transplant. 1994; 8: 358-364PubMed Google Scholar found anemia (defined as hematocrit < 38% in men and < 35% in women) in 80% of their subjects 2 weeks after transplantation. At 1 year of follow-up, this figure decreased to 29%. Using different thresholds for defining anemia (hemoglobin < 11 g/dL [<110 g/L] for women and < 12 g/dL [<120 g/L] for men), Shibagaki and Shetty21Shibagaki Y. Shetty A. Anemia is common after kidney transplantation, especially among African Americans.Nephrol Dial Transplant. 2004; 19: 2368-2373Crossref PubMed Scopus (43) Google Scholar reported a 20% prevalence of severe anemia in a series of 192 transplant recipients. Similarly, Mix et al22Mix T.C. Kazmi W. Khan S. et al.Anemia: A continuing problem following kidney transplantation.Am J Transplant. 2003; 3: 1426-1433Crossref PubMed Scopus (135) Google Scholar studied 240 renal transplant recipients and found hematocrits less than 36% (corresponding to hemoglobin level of about <12 g/dL [<120 g/L]) in 76% of patients at the time of transplantation and 21% and 36% at 1 and 4 years postengraftment, respectively. In addition, they reported a surprising lack of investigation and intervention; even in subjects with a hematocrit less than 30%, only 46% had undergone any investigation for iron repletion status and only 40% had been prescribed an erythropoiesis-stimulating agent.22Mix T.C. Kazmi W. Khan S. et al.Anemia: A continuing problem following kidney transplantation.Am J Transplant. 2003; 3: 1426-1433Crossref PubMed Scopus (135) Google Scholar The magnitude of the problem is confirmed by the publication of Lorenz et al,23Lorenz M. Kletzmayr J. Perschl A. et al.Anemia and iron deficiencies among long-term renal transplant recipients.J Am Soc Nephrol. 2002; 13: 794-797PubMed Google Scholar primarily a study of iron status post–renal transplantation. They reported a figure as high as 39.7% for anemia in their cohort of 438 engrafted individuals by using WHO criteria,23Lorenz M. Kletzmayr J. Perschl A. et al.Anemia and iron deficiencies among long-term renal transplant recipients.J Am Soc Nephrol. 2002; 13: 794-797PubMed Google Scholar similar to the 34% in the recent report of Molnar et al24Molnar M.Z. Novak M. Ambrus C. et al.Anemia in kidney transplanted patients.Clin Transplant. 2005; 19: 825-833Crossref PubMed Scopus (50) Google Scholar (again using WHO criteria). In children, anemia after renal transplantation also appears to be more common than might have been imagined (for a comprehensive review, see25Al-Uzri A. Yorgin P.D. Kling P.J. Anemia in children after transplantation: Etiology and the effect of immunosuppressive therapy on erythropoiesis.Pediatr Transplant. 2003; 7: 253-264Crossref PubMed Scopus (51) Google Scholar). For example, a cross-sectional analysis26Kausman J.Y. Powell H.R. Jones C.L. Anemia in pediatric renal transplant recipients.Pediatr Nephrol. 2004; 19: 526-530Crossref PubMed Scopus (40) Google Scholar of 50 pediatric transplant recipients observed a mean hemoglobin level of 11.0 g/dL (110 g/L) and anemia prevalence of 60% (defined as hemoglobin < 11 g/dL [<110 g/L] for children aged 2 to 6 years, <11.5 g/dL [<115 g/L] for those aged 6 to 12 years, and < 12 g/dL [<120 g/L] for children > 12 years). The study of Yorgin et al27Yorgin P. Belson A. Sanchez J. et al.Unexpectedly high prevalence of posttransplant anemia in pediatric and young adult renal transplant recipients.Am J Kidney Dis. 2002; 40: 1306-1318Abstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar suggested an even greater prevalence of 64% to 82% in pediatric subjects from 1 to 5 years posttransplantation. Taking all these (and many other) studies together and allowing for the caveats invoked earlier, it is likely that approximately one third of transplant recipients are anemic at any one time. Taking the transplant recipients’ clinical journey, it is likely that up to two thirds of transplant recipients are anemic at some stage. It also appears that investigation and intervention are not (yet) the norm. A useful construct for considering anemia in the posttransplantation setting is to divide it into anemia that develops early (in the first 6 months) and that which develops late (after the first 6 months) postengraftment. Although considerable overlap occurs, this distinction is important when considering causes for posttransplantation anemia because certain risk factors are more likely to have a part at some times than at others. Table 2 lists the many potential causes of posttransplantation anemia by cause. As can be seen, some factors are shared with patients with CKD who did not undergo transplantation (such as impaired kidney function, iron and nutrient deficiency, infection, inflammation, blood loss, and medications [eg, angiotensin-converting enzyme (ACE) inhibitors]), whereas others are unique to transplant recipients (eg, rejection episodes, immunosuppressive drugs, antivirals, antibiotics, and malignancy). In most cases, causation is likely to be multifactorial, and there is considerable interplay of risk factors. Cases to illustrate this are shown in Figs 1 (early) and 2 (late posttransplantation anemia). Recent surveys are suggestive that both early and late posttransplantation anemia is becoming more common.18Vanrenterghem Y. Ponticelli C. Morales J.M. et al.Prevalence and management of anemia in renal transplant recipients: A European survey.Am J Transplant. 2003; 3: 835-845Crossref PubMed Scopus (262) Google Scholar, 19Vanrenterghem Y. Anemia after renal transplantation.Nephrol Dial Transplant. 2004; 19: SV54-SV58Google ScholarTable 2Causes of Posttransplantation AnemiaEarly Generalized bone marrow suppression Immunosuppressants: AZA, MMF, sirolimus Antibacterials/antivirals: chloramphenicol, ganciclovir, trimethoprim-sulfamethoxazole Viral infections: CMV, Epstein-Barr virus, human immunodeficiency virus, human parvovirus B19 PRCA Drug related: AZA, MMF, tacrolimus, ACE inhibitors Infection related: parvovirus B19 Hemolytic uremic syndrome/hemolytic anemia Drug related: cyclosporine, tacrolimus, sirolimus Hematologic: ABO incompatibility, sickle cell disease, glucose 6 phosphate dehydrogenase deficiency Acute renal failure Acute tubular necrosis Acute rejection Iron deficiency Absolute: perioperative blood loss, stress-induced gastrointestinal hemorrhage, depleted iron stores Functional: chronic inflammation, uremia Folate and vitamin B12 deficiencyLate Generalized bone marrow suppression Immunosuppressants: AZA, MMF, sirolimus PRCA Drug related: AZA, MMF, tacrolimus, ACE inhibitors Hemolytic uremic syndrome/hemolytic anemia Drug related: cyclosporine, tacrolimus, sirolimus Hematologic: ABO incompatibility, sickle cell disease, glucose 6 phosphate dehydrogenase deficiency Acute renal failure Acute tubular necrosis Acute rejection Chronic renal failure EPO deficiency EPO resistance: eg, chronic inflammation, hyperparathyroidism Iron deficiency Absolute: perioperative blood loss, stress-induced gastrointestinal hemorrhage, depleted iron stores Functional: Uremia, chronic inflammation Malignancy Folate and vitamin B12 deficiencyNOTE. A useful way of considering posttransplantation anemia is to divide it into that which develops early (within the first 6 months) and late (after the first 6 months) postengraftment. Some causes of posttransplantation anemia can occur either early or late. Open table in a new tab Fig 2Late posttransplantation anemia; evolution of hemoglobin concentration from 13 to 70 months postengraftment in the same patient as Fig 1. Renal transplant function was stable, with serum creatinine level around 1.6 mg/dL (142 μmol/L) on cyclosporine, AZA, and prednisolone therapy. Hemoglobin level briefly reached 16.3 g/dL (163 g/L; hematocrit, 54%). However, serum creatinine levels slowly deteriorated from 14 to 50 months postengraftment, reaching 2.2 mg/dL (195 μmol/L). A renal biopsy was performed, showing CAN. Cyclosporine therapy was discontinued in favor of sirolimus, started at month 52. Although serum creatinine level improved to 1.8 mg/dL (160 μmol/L), hemoglobin level decreased quickly from 15.5 g/dL (155 g/L) in month 50 to 9.4 g/dL (94 g/L) in month 61. Sirolimus therapy was discontinued at month 61 (because of skin rash, edema, dyslipidemia, and anemia), and MMF was substituted. Only a small increase in hemoglobin levels followed. Iron status was normal throughout. To convert serum creatinine in μmol/L to mg/dL, divide by 88.4; hemoglobin in g/dL to g/L, multiply by 10.View Large Image Figure ViewerDownload (PPT) NOTE. A useful way of considering posttransplantation anemia is to divide it into that which develops early (within the first 6 months) and late (after the first 6 months) postengraftment. Some causes of posttransplantation anemia can occur either early or late. There are potentially very rare, but well-characterized, causes for profound anemia, including infection with parvovirus B1928Garewal G. Ahluwalia J. Varma N. et al.Parvovirus B19 infection-associated red-cell aplasia in renal-transplant recipients: Clues from the bone marrow.Transplantation. 2004; 77: 320-321Crossref PubMed Scopus (16) Google Scholar and thrombotic microangiopathy secondary to calcineurin-inhibitor or sirolimus therapy.29Robson M. Cote I. Abbs I. et al.Thrombotic micro-angiopathy with sirolimus-based immunosuppression: Potentiation of calcineurin-inhibitor-induced endothelial damage?.Am J Transplant. 2003; 3: 324-327Crossref PubMed Scopus (88) Google Scholar However, a number of common risk factors for posttransplantation anemia have emerged consistently from a series of studies (including those cited). These include recipient sex, race, renal function, iron depletion, cytomegalovirus (CMV) status and prophylaxis, donor age, immunosuppressive regimen, use of ACE inhibitors/angiotensin II receptor blockers (ARBs), and others. Of these, the factor that appears to exert the greatest influence on anemia prevalence and severity is renal function/eGFR. For example, Karthikeyan et al30Karthikeyan V. Karpinski J. Nair R.C. et al.The burden of chronic kidney disease in renal transplant recipients.Am J Transplant. 2004; 4: 262-269Crossref PubMed Scopus (125) Google Scholar determined the prevalence of CKD in 459 renal transplant recipients who were at least 6 months posttransplantation (mean, 7.7 years). CKD was present in 412 of these patients (60% had CKD stage 3). By stage 3, a total of 28.6% of patients were administered recombinant human EPO (rHuEPO; 6.6%) or had a hemoglobin level less than 11 g/dL (<110 g/L; 22%). This increased to 27% and 33% for stage 4 patients and 33% and 50% for stage 5 patients.30Karthikeyan V. Karpinski J. Nair R.C. et al.The burden of chronic kidney disease in renal transplant recipients.Am J Transplant. 2004; 4: 262-269Crossref PubMed Scopus (125) Google Scholar Our own findings31Shah N. Al-Khoury S. Afzali B. et al.Post-transplantation anaemia in adult renal allograft recipients—Prevalence and predictors.Transplantation. 2006; 81: 1112-1118Crossref PubMed Scopus (101) Google Scholar in a population of 1,511 transplant recipients identified renal function as the strongest individual predictor of hemoglobin level (r = 0.33; P < 0.0001). It is important to appreciate that kidney transplant recipients have decreased kidney function and thus are at risk for anemia. Nevertheless, for most renal transplant recipients, eGFR is approximately 50 to 60 mL/min (0.83 to 1 mL/s) in the first year after renal transplantation, equating to KDOQI CKD stages 2 to 3.32Marcen R. Pascual J. Tenorio M. et al.Chronic kidney disease in renal transplant recipients.Transplant Proc. 2005; 37: 3718-3720Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar In the absence of other pathological states, anemia in nontransplantation patients with CKD would not be expected to be significant at this level of renal function (although clearly exceptions occur), highlighting the existence of risk factors other than GFR in the transplantation setting. An alternative explanation that should be borne in mind is that estimates of GFR derived from creatinine-based calculations might not be correct in transplant recipients (the Modification of Diet in Renal Disease equation has not been validated in transplant recipients), potentially leading to misclassifications of CKD stage. Nevertheless, in the TRESAM Study, epidemiological characteristics of the population suggested a strong association between allograft function and anemia, but subjects who received a second or third allograft were mor" @default.
• W2078993832 created "2016-06-24" @default.
• W2078993832 creator A5036599201 @default.
• W2078993832 creator A5039962473 @default.
• W2078993832 creator A5042602459 @default.
• W2078993832 creator A5046429359 @default.
• W2078993832 creator A5049079690 @default.
• W2078993832 creator A5051811277 @default.
• W2078993832 date "2006-10-01" @default.
• W2078993832 modified "2023-09-26" @default.
• W2078993832 title "Anemia After Renal Transplantation" @default.
• W2078993832 cites W1514806186 @default.
• W2078993832 cites W1582424828 @default.
• W2078993832 cites W1963923905 @default.
• W2078993832 cites W1966106544 @default.
• W2078993832 cites W1967490229 @default.
• W2078993832 cites W1970517319 @default.
• W2078993832 cites W1971128957 @default.
• W2078993832 cites W1974750082 @default.
• W2078993832 cites W1975736471 @default.
• W2078993832 cites W1977002434 @default.
• W2078993832 cites W1979155203 @default.
• W2078993832 cites W1979816146 @default.
• W2078993832 cites W1982946518 @default.
• W2078993832 cites W1984199451 @default.
• W2078993832 cites W1991016726 @default.
• W2078993832 cites W1993024767 @default.
• W2078993832 cites W1994434656 @default.
• W2078993832 cites W1995817487 @default.
• W2078993832 cites W1998038903 @default.
• W2078993832 cites W1999621949 @default.
• W2078993832 cites W2004411859 @default.
• W2078993832 cites W2007555319 @default.
• W2078993832 cites W2009276456 @default.
• W2078993832 cites W2010005807 @default.
• W2078993832 cites W2010211071 @default.
• W2078993832 cites W2018384104 @default.
• W2078993832 cites W2019455207 @default.
• W2078993832 cites W2020820828 @default.
• W2078993832 cites W2021142445 @default.
• W2078993832 cites W2031181083 @default.
• W2078993832 cites W2032992784 @default.
• W2078993832 cites W2033631884 @default.
• W2078993832 cites W2034045687 @default.
• W2078993832 cites W2035360618 @default.
• W2078993832 cites W2036048816 @default.
• W2078993832 cites W2039913375 @default.
• W2078993832 cites W2040299750 @default.
• W2078993832 cites W2042681264 @default.
• W2078993832 cites W2044068240 @default.
• W2078993832 cites W2045098873 @default.
• W2078993832 cites W2046506563 @default.
• W2078993832 cites W2055982220 @default.
• W2078993832 cites W2059444951 @default.
• W2078993832 cites W2067103756 @default.
• W2078993832 cites W2072314403 @default.
• W2078993832 cites W2072896804 @default.
• W2078993832 cites W2074964477 @default.
• W2078993832 cites W2076292769 @default.
• W2078993832 cites W2079165129 @default.
• W2078993832 cites W2080404930 @default.
• W2078993832 cites W2081858766 @default.
• W2078993832 cites W2082771638 @default.
• W2078993832 cites W2083003822 @default.
• W2078993832 cites W2087792355 @default.
• W2078993832 cites W2088466196 @default.
• W2078993832 cites W2091799246 @default.
• W2078993832 cites W2093711374 @default.
• W2078993832 cites W2094193505 @default.
• W2078993832 cites W2098974363 @default.
• W2078993832 cites W2099085184 @default.
• W2078993832 cites W2099348212 @default.
• W2078993832 cites W2102922663 @default.
• W2078993832 cites W2109081740 @default.
• W2078993832 cites W2114657900 @default.
• W2078993832 cites W2116534420 @default.
• W2078993832 cites W2120073730 @default.
• W2078993832 cites W2123940335 @default.
• W2078993832 cites W2128110354 @default.
• W2078993832 cites W2132072950 @default.
• W2078993832 cites W2133518765 @default.
• W2078993832 cites W2134113483 @default.
• W2078993832 cites W2135618051 @default.
• W2078993832 cites W2144061653 @default.
• W2078993832 cites W2147032364 @default.
• W2078993832 cites W2151606421 @default.
• W2078993832 cites W2157195541 @default.
• W2078993832 cites W2160463464 @default.
• W2078993832 cites W2160581087 @default.
• W2078993832 cites W2167124746 @default.
• W2078993832 cites W2169588753 @default.
• W2078993832 cites W2170231310 @default.
• W2078993832 cites W2171844927 @default.
• W2078993832 cites W2280610749 @default.
• W2078993832 cites W2313706101 @default.
• W2078993832 cites W2323589684 @default.
• W2078993832 cites W2442254849 @default.
• W2078993832 cites W2495747826 @default.

• next