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Abstract: TH-PO948

Successful Treatment of Anemia with Roxadustat in a Hemodialysis Patient Following Erythropoietin-Induced Pure Red Cell Aplasia

Session Information

Category: Anemia and Iron Metabolism

  • 200 Anemia and Iron Metabolism


  • Pai, Pearl, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China
  • Ma, Xuejuan, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China
  • Chen, Xiaowei, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China
  • Zhu, Wenjuan, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China
  • Cui, Liwen, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China

Erythropoietin (EPO) antibody (Ab)-induced Pure Red Cell Aplasia (PRCA) is a rare condition. Treatment usually requires immediate withdrawal of EPO and treatment with immunosuppression or renal transplantation. Here, we present the successful treatment of a case of EPO Ab-induced PRCA with cyclosporin (CyA) and Roxadustat, a hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI).

Case Description

A 58-year-old man developed kidney failure as a result of diabetes mellitus. In July 2021, shortly before he began dialysis, he was commenced rHuEPO (Jimaixin, epoetin-α, KexingBio, Shandong, China) subcutaneously 5000 IU twice a week. He began hemodialysis (HD) in November 2021. He was switched to intravenous rHuEPO (6000 IU) (Yipuding, epoetin-α, NCPC GenetechBio, Hebei, China) once a week. His Hb increased to 116 g/L in the first 3 months but fell to 75 g/L 6 months into HD. 3½ weeks later, he presented with a pneumonia and a Hb of 48 g/L. He was treated with antibiotics and was transfused. His EPO was stopped. He was started on Roxadustat. 18 days later, his Hb fell to 38 g/L, his reticulocytes was 2900/uL. A bone marrow (BM) biopsy showed a proliferative active BM but reduced erythropoiesis and an erythroid precursor of 7%. A diagnosis of EPO Ab-induced PRCA was suspected. However, an anti-EPO Ab ELISA test later turned out negative. Some likely causes of PRCA such as lymphoproliferative disorder, parvovirus B19 infection, thymoma and systemic autoimmune disease were excluded. The Roxadustat was discontinued. A second BM biopsy showed a erythroid precursors of 5.2%. The suspicion of a EPO Ab-induced PRCA was maintained. The patient was commenced CyA 3mg/kg/day and was given 25 more units of blood over 2 months. The reticulocyte counts took 3 months to recover to normal. The patient was recommenced on Roxadustat 100 mg TIW and his Hb stabilized.


Even though the anti-EPO Ab was negative by ELISA assay in our case, the clinical course, with markedly reduced reticulocyte count <10000/ul, a BM biopsy revealing reduced erythroblasts only, and its subsequent response to CyA, were in keeping with EPO Ab-induced PRCA. Anti EPO Ab assay is not always positive in EPO Ab-induced PRCA. Our case illustrates that treatment with Cyclosporin and a switch to Roxadustat are useful in treating EPO Ab-induced PRCA.