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* Department of Medicine, Royal North Shore Hospital, University of Sydney, St. Leonards, NSW; Departments of Renal Medicine and Internal Medicine, University of Queensland at Princess Alexandra Hospital, Brisbane, Australia; Division of Nephrology and Dialysis, Medical University of Vienna, Vienna, Austria; Amgen Global Safety, Amgen, Uxbridge, United Kingdom; || Service d’Immunologie et d’Hematologie, INSERM, U790 Institut Gustave Roussy, Villejuif, and AP-HP, Hôpital Saint Antoine and Université Pierre et Marie Curie, Paris, France; ¶ Department of Innovation Studies, Central Laboratory, Animal Institute, Utrecht University, Utrecht, Netherlands; ** Hospital de L’Enfant Jesus, Université Laval, Département de Médicine, Québec City, Québec, Canada; Servicio de Nefrologia, Hospital Universitario Marqués de Valdecilla, Santander, Spain; Renal Unit, Kings College Hospital, London, United Kingdom; National Institute for Biological Standards and Control, Division of Immunology and Endocrinology, Hertfordshire, United Kingdom; and |||| Nephrology, Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada
Correspondence: Dr. Carol Pollock, Department of Medicine, Royal North Shore Hospital, University of Sydney, Department of Medicine, Pacific Highway, Street Leonards, NSW, 2065, Australia. Phone: 61-2-9926-7126; Fax: 61-2-9436-3719; E-mail: carpol{at}med.usyd.edu.au
Pure red cell aplasia in patients who are treated for anemia of chronic kidney disease with erythropoiesis-stimulating agents such as epoetin was first reported in 1998. Although the incidence of pure red cell aplasia peaked in 2002, it remains important for nephrologists to know how to investigate a suspected case of pure red cell aplasia and how to identify other causes of hyporesponsiveness to erythropoiesis-stimulating agents, which account for the vast majority of such cases. The authors reviewed the current status of information in the literature and drew on their personal experiences with patients regarding the diagnosis and management of epoetin-induced pure red cell aplasia. The mechanism for development of epoetin-induced pure red cell aplasia remains unconfirmed. It generally occurs after the production of neutralizing anti-erythropoietin antibodies. Elucidation of a suspected pure red cell aplasia case requires a systematic approach, beginning with simple measurements such as blood cell counts, because most cases of erythropoiesis-stimulating agent hyporesponsiveness are attributable to other causes. If these criteria indicate that the patient's response to erythropoiesis-stimulating agent therapy is very poor, then bone marrow examination and measurement of anti-erythropoietin antibodies is justified. If pure red cell aplasia is confirmed, then cessation of erythropoiesis-stimulating agent therapy and initiation of immunosuppressive therapy are recommended. Continued study of epoetin-induced pure red cell aplasia is needed to help nephrologists prevent or manage future cases and will have implications for the use of other protein-based therapeutic agents.
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