Recovery from Pure Red Cell Aplasia Caused by Anti Erythropoietin Antibodies After Kidney Transplantation

Snanoudj, Renaud; Beaudreuil, Séverine; Arzouk, Nadia; Jacq, D; Casadevall, Nicole; Charpentier, B; Dürrbach, Antoine

doi:10.1046/j.1600-6143.2003.00297.x

Cited by 16 publications

(9 citation statements)

References 13 publications

(15 reference statements)

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“…A more recent study concurred with these findings, showing an increased EPO concentration (in the absence of exogenous administration) in anemic patients compared with nonanemic patients after transplantation (20). It is interesting that it has been documented that anti-EPO antibodies that occasionally are responsible for severe anemia before transplantation tend to disappear after initiation of immunosuppression at the time of transplantation (21).…”

Section: Causes and Correlatesmentioning

confidence: 68%

Pottransplantation Anemia

Winkelmayer

Chandraker²

2008

Clinical Journal of the American Society of Nephrology

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In recent years, there has been an increasing interest in studying the anemia that occurs after kidney transplantation. Although many of the guidelines for the treatment of kidney transplant patients, including those for anemia, are extrapolated from recommendations for patients with chronic kidney disease, there are important differences in the cause of and response to anemia in kidney transplant recipients. In addition to the correlation of anemia with kidney function as in native renal disease, many other factors are associated with the development of anemia after transplantation, including the use of medications and the inflammation/immune response. Given the lack of large, well-designed, prospective studies, the consequences of anemia, the response to treatment, and the cost-effectiveness of treatment in the posttransplantation setting are also poorly understood.Clin J Am Soc Nephrol 3: S49 -S55, 2008S49 -S55, . doi: 10.2215 A lthough anemia has been investigated with great interest and intensity in patients with chronic kidney disease (CKD), including the dialysis population, studies of the prevalence and clinical relevance of posttransplantation anemia (PTA) were scarce until a few years ago. One could argue that patients with a functioning kidney transplant are similar to patients with chronic native renal insufficiency (not on dialysis) and that evidence from the CKD population could be extrapolated to these kidney transplant recipients (KTR) (1). There are, however, at least three important reasons that such an extrapolation may not be legitimate: The presence of immunosuppressant agents and other transplant-related medications, the altered inflammatory milieu, and the history of prolonged maintenance dialysis therapy in most KTR. The altered inflammatory milieu is due to the systemic immune response to the presence of alloantigen, leading to a proinflammatory state that increases erythropoietin (EPO) resistance. Inadequate dialysis and activation of cytokines by dialysis membranes have also been shown to cause EPO resistance, but whether these factors have long-term consequences that carry over after transplantation are unknown. These and other factors may confound the validity of extrapolating scientific findings and clinical experience from the CKD (not on dialysis) population. Thus, it seems essential to establish evidence directly from the KTR population rather than through inference from patients with CKD. This article provides a critical review of the evidence on PTA. Course of Anemia after TransplantationTwo major developments have influenced the degree of anemia in patients with renal failure at the time of transplantation. The first is the widespread use of EPO for dialysis patients and patients with CKD. This has had the effect of reducing the degree of anemia in potential transplant recipients and decreased the likelihood of immunologic sensitization in patients as a result of the decreased need for blood transfusions before transplantation. Although decreasing the number of blood transfus...

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Section: Causes and Correlatesmentioning

confidence: 68%

Pottransplantation Anemia

Winkelmayer

Chandraker²

2008

Clinical Journal of the American Society of Nephrology

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“…17,18 Other studies have revealed that despite the new therapeutic and clinical approaches, the survival rate remains unsatisfactory. 19,20 The patient in the present report received a regimen of high doses of steroids (dexamethasone, 40 mg) in association with a proteosome inhibitor (bortezomib, 0.7 mg/m 2 ), and despite its toxicity, it led the patient to a good response with good tolerance, and an increase in the patient's quality of life. Because he presented stage V renal disease with hemodialysis support, age above 65 years and slightly increased basal brain natriuretic peptide, the patient did not fulfill the criteria for stem cell transplantation and was classified as high risk.…”

Section: Discussionmentioning

confidence: 84%

Renal failure due to primary amyloidosis: a case report and literature review

et al. 2011

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CONTEXT: Primary amyloidosis, also known as AL amyloidosis, is commonly caused by clonal expansion of plasma cells in the bone marrow, thereby segregating light chains of clonal immunoglobulin that settle in tissues in the form of insoluble amyloid fibrils. The aim of this study was to report a case of primary amyloidosis with renal failure, diagnosed in Hospital São João, Porto, Portugal, focusing on the diagnostic difficulties and presenting a literature review. CASE REPORT:A 68-year-old Caucasian man was admitted to the Internal Medicine Department of the hospital with a condition of anasarca and nephrotic syndrome. After performing a renal biopsy that tested positive using Congo red and immunohistochemistry, lambda light chain amyloidosis was diagnosed. This evolved into terminal renal disease, which led to hemodialysis and several episodes of urinary and catheter infections. He was started on chemotherapy, consisting of bortezomib 0.7 mg/m 2 and dexamethasone 40 mg in six cycles. This led to clinical improvement, stabilization of the illness and good tolerance of the treatment.CONCLUSION: Amyloidosis is a rare entity that is difficult to diagnose. This is because of the unspecific early clinical manifestations of the disease.The hypothesis of amyloidosis is only considered when specific organ failure occurs. This case consisted of primary amyloidosis with involvement of the kidneys as an initial presentation of the disease and its difficulties were shown, going from the clinical approach to the final diagnosis. RESUMOCONTEXTO: A amiloidose primária, também conhecida como amiloidose AL, é geralmente causada pela expansão clonal de plasmócitos na medula óssea que segregam cadeias leves de imunoglobulina clonal, as quais se depositam nos tecidos na forma de fibrilas amiloides insolúveis. O objetivo deste estudo é relatar um caso de amiloidose primária com acometimento renal diagnosticado no Hospital São João, Porto, Portugal, enfatizando as dificuldades do diagnóstico e apresentando uma revisão da literatura.RELATO DO CASO: Homem de 68 anos, branco, foi admitido no Serviço de Medicina Interna do hospital com quadro de anasarca e síndrome nefrótica. Após realizar biópsia renal, que foi positiva para o vermelho congo e imunoistoquímica, foi diagnosticada amiloidose de cadeia leve lambda. Evoluiu para doença renal terminal, o que levou a hemodiálise e tendo vários episódios de infecções urinárias e do cateter. Iniciou a quimioterapia com bortezimib, 0,7 mg/m 2 , e dexametasona, 40 mg em seis ciclos, levando a uma melhoria clínica, a estabilização da doença e boa tolerância ao tratamento.CONCLUSÃO: Amiloidose consiste em uma entidade rara e de difícil diagnóstico. Isso ocorre devido a manifestações clínicas da doença pouco específicas, e esta hipótese só é considerada quando do acometimento de um órgão em particular. O caso em questão refere-se a uma apresentação da amiloidose primária com envolvimento renal, como apresentação clínica inicial da doença, e as dificuldades desde a abordagem clínica até o dia...

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“…In a retrospective survey of 47 patients with erythropoietin‐induced PRCA, 37 received immunosuppressive therapy and 78% of these patients were cured of PRCA. Renal transplantation was associated with cure of PRCA in all of the reported patients (6, 12, 13). The course of the disease in our patient differs significantly from other reports in the literature.…”

Section: Discussionmentioning

confidence: 85%

Prolonged course of pure red cell aplasia after erythropoietin therapy

Nigg¹,

Schanz²,

Ambühl³

et al. 2004

European J of Haematology

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Pure red cell aplasia (PRCA) caused by neutralising anti-erythropoietin antibodies is a very rare disease. Since 1998, an increased incidence of PRCA in patients with kidney failure following treatment with recombinant human erythropoietin (rhEpo) has been reported, mostly in Europe. In most cases, PRCA was cured by immunosuppressive therapy, immunoglobulins, plasmapheresis or renal transplantation. We report an exceptionally prolonged course of PRCA over 68 months despite renal transplantation and different immunosuppressive regimens.

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Recovery from Pure Red Cell Aplasia Caused by Anti Erythropoietin Antibodies After Kidney Transplantation

Cited by 16 publications

References 13 publications

Pottransplantation Anemia

Pottransplantation Anemia

Renal failure due to primary amyloidosis: a case report and literature review

Prolonged course of pure red cell aplasia after erythropoietin therapy

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