Febuxostat for hyperuricemia: experience with patients on chronic hemodialysis treatment

Abstract

To the Editor Febuxostat a non-purine xanthine oxidase inhibitor, which recently received marketing approval, has used as an option for the treatment of hyperuricemia because it undergoes hepatic metabolism and may require less dose adjustment in association with renal function [1]. However, information regarding the therapeutic benefit of such an agent among chronic kidney disease (CKD) patients is limited. We would like to present our experience with five cases of chronic hemodialysis (HD) patients whose hyperuricemia was successfully treated by oral febuxostat with no apparent adverse events. All patients were male with an average age of 66.6 ± 18.5 years. No urate lowering agents (ULTs) had been used in the three out of five patients and the other two patients were switched from oral allopurinol to febuxostat. No one reported previous gout attacks. Patients 1–3 were placed on 10 mg febuxostat daily, while patients 4 and 5 were administered 20 mg/day febuxostat. The average values of the serum uric acid (UA) levels just before and after the initiation of oral febuxostat were 10.1 ± 0.9 mg/dl (mean ± SD) and 6.2 ± 0.9 mg/dl (p = 0.0014), respectively (Fig. 1). No acute gout flares were reported during a four-month follow-up, and the serum UA level remained at most around 6.0 mg/dl without any significant changes in laboratory profiles and clinical signs. Patient 5 showed a marked reduction in serum UA level to 1.3 mg/dl, and febuxostat was discontinued, and his serum UA levels were finally maintained around 4.0–6.0 mg/dl by febuxostat with a post dialysis dose of 10 mg three times a week. The current observations suggest that even relatively low doses of febuxostat, which is approved at a dose of 40–60 mg/day as the standard dosages for the treatment of hyperuricemia with gouty arthritis in Japan, may work effectively among chronic HD patients for the prompt reduction of serum UA at a level that has been arbitrarily proposed as a therapeutic target for hyperuricemia [2, 3]. R. Horikoshi M. Inoue Division of Nephrology, Department of Internal Medicine, Ibaraki Prefectural Central Hospital, Kasama, Ibaraki, Japan