title: Pure red cell aplasia induced by erythropoiesis-stimulating agents.
abstract: 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.
authors.affiliation: Department of Medicine, Royal North Shore Hospital, University of Sydney, Department of Medicine, Pacific Highway, Street Leonards, NSW, 2065, Australia. carpol@med.usyd.edu.au
authors.forename: Carol
authors.initials: C
authors.lastname: Pollock
authors.forename: David Wayne
authors.initials: DW
authors.lastname: Johnson
authors.forename: Walter H
authors.initials: WH
authors.lastname: Hörl
authors.forename: Jerome
authors.initials: J
authors.lastname: Rossert
authors.forename: Nicole
authors.initials: N
authors.lastname: Casadevall
authors.forename: Huub
authors.initials: H
authors.lastname: Schellekens
authors.forename: Robert
authors.initials: R
authors.lastname: Delage
authors.forename: Angel
authors.initials: A
authors.lastname: De Francisco
authors.forename: Iain
authors.initials: I
authors.lastname: Macdougall
authors.forename: Robin
authors.initials: R
authors.lastname: Thorpe
authors.forename: Edwin
authors.initials: E
authors.lastname: Toffelmire
mesh_terms: D000740:Anemia / Q000188:drug therapy* / Q000209:etiology; D000906:Antibodies; D004921:Erythropoietin / Q000009:adverse effects* / Q000276:immunology; D006397:Hematinics / Q000009:adverse effects* / Q000276:immunology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications*; D012010:Red-Cell Aplasia, Pure / Q000139:chemically induced* / Q000473:pathology
chemical_list: D000906:Antibodies; D006397:Hematinics; D004921:Erythropoietin