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      Prevalence of Anti-Erythropoietin Antibodies in Hemodialysis Patients without Clinical Signs of Pure Red Cell Aplasia

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          Background/Aims: The prevalence of anti-erythropoietin antibodies in renal patients without clinical evidence of pure red cell aplasia (PRCA) who respond poorly to epoetin is unknown. This study tested for anti-erythropoietin antibodies in hemodialysis patients who were either hypo- or normoresponsive to epoetin treatment. Methods: Epoetin hyporesponsiveness (hemoglobin ≤10.5 g/dl and epoetin ≧9,000 IU/week) and normoresponsiveness (hemoglobin >10.5 g/dl and epoetin <7,000 IU/week) were arbitrarily defined. Prevalence of anti-erythropoietin antibodies in hemodialysis patients without symptoms of PRCA was determined by screening sera of 536 patients from 35 German KfH dialysis units, using enzyme-linked immunosorbent assay (ELISA). Positive results were verified by radioimmunoprecipitation assay (RIP) and neutralizing activity was determined by bioassay. Results: Anti-erythropoietin antibodies were detected in 3 hyporesponsive and 3 normoresponsive patients using ELISA. One patient per group was verified as borderline by RIP testing; the other 4 were negative. The bioassay was negative for 1 patient; the other died unrelated to PRCA before testing. Follow-up with RIP testing after 15 months under continuous epoetin treatment was negative (4 patients, 2 deceased). Conclusion: This survey did not identify anti-erythropoietin antibodies in hemodialysis patient’s hyporesponsive to epoetin and does not support presumptive antibody screening as a routine work-up in these patients.

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          Most cited references 16

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          Autoantibodies against erythropoietin in a patient with pure red-cell aplasia.

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            Treatment of erythropoietin-induced pure red cell aplasia: a retrospective study.

            Recombinant human erythropoietin is the standard treatment for anaemia related to chronic kidney disease, and its widespread use has been favoured by a very high therapeutic index. However, since 1998, more than 200 patients worldwide with chronic kidney disease treated in this way have developed neutralising antibodies to erythropoietin, causing pure red cell aplasia. We aimed to collate clinical and pathological features in patients unequivocally shown to have erythropoietin-induced pure red cell aplasia. We retrospectively obtained data from the files of 47 patients with pure red cell aplasia. We assessed treatment and outcome of patients and defined recovery from pure red cell aplasia as an increase in reticulocyte counts to more than 20 000 per microL in patients who were no longer transfusion-dependent. When patients developed pure red cell aplasia, all were receiving erythropoietin subcutaneously, and the product most typically prescribed was epoetin alfa (Eprex, Ortho Biotech). The median delay between start of erythropoietin treatment and occurrence of pure red cell aplasia was 11 months (IQR 7.5-14). Nine patients received no immunosuppressive treatment, and none of these recovered. Of 37 patients who received immunosuppressive therapy, 29 (78%) recovered. All six patients who received a kidney transplant recovered within 1 month, and recovery rates were between 56% and 88% in patients treated with corticosteroids, corticosteroids plus cyclophosphamide, or ciclosporin. No relapse of pure red cell aplasia happened after stopping immunosuppressive treatment, but no patient was rechallenged with erythropoietin. Immunosuppressive treatment accelerates recovery from erythropoietin-induced pure red cell aplasia.
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              Pure red-cell aplasia due to anti-erythropoietin antibodies.


                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                January 2007
                12 December 2006
                : 105
                : 2
                : c90-c98
                aDepartment of Internal Medicine, Division of Nephrology, University Hospital of Cologne, bInstitute of Health Economics, University of Cologne, Cologne, and cInstitute of Immunology, Clinical Pathology, Molecular Medicine, Hamburg, Germany
                97889 Nephron Clin Pract 2007;105:c90–c98
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 3, References: 26, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/97889
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