Roxadustat as treatment for a blood transfusion-dependent maintenance hemodialysis patient: A case report and review of literature

paythelady.612 shared this article with you from Inoreader Roxadustat as treatment for a blood transfusion-dependent maintenance hemodialysis patient: A case report and review of literature Μέσω pubmed: "world j clin cases"... World J Clin Cases. 2021 May 26;9(15):3680-3688. doi: 10.12998/wjcc.v9.i15.3680. ABSTRACT BACKGROUND: Erythropoiesis-stimulating agents (ESAs) have revolutionized the therapeutic strategy for anemia in chronic kidney disease. However, some cases are resistant or hyporesponsive to ESAs. Roxadustat is an oral hypoxia-inducible factor-prolyl hydroxylase inhibitor that stimulates erythropoiesis and regulates iron metabolism. Here, we describe a hemodialysis patient with refractory anemia who did not respond to traditional treatments and depended on blood transfusion for more than 1 year. After applying Roxadustat, the patient's anemia improved significantly. CASE SUMMARY: A 44-year-old man was diagnosed with uremia accompanied by severe anemia with a hemoglobin (Hb) level ranging from 30-40 g/L. His anemia did not improve after sufficient dialysis or high doses of active ESAs; other causes of anemia were excluded. The patient require d approximately 600-1000 mL of red blood cell suspension every 15-30 d for more than 1 year. After accepting Roxadustat therapy, the patient's anemia symptoms improved significantly; his Hb level gradually increased to 50 g/L, and no further blood transfusions were administered. His Hb level reached 69 g/L by the 34th week. Although a Hb level of 60-70 g/L cannot be considered satisfactory, he no longer required blood transfusions and his quality of life was substantially improved. Roxadustat showed good efficacy and safety in this case. CONCLUSION: Roxadustat represents an innovative and effective agent for the clinical treatment of renal anemia caused by multiple complex factors. PMID:34046470 | PMC:PMC8130086 | DOI:10.12998/wjcc.v9.i15.3680 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.