Abstract
BackgroundCurrently, hyperuricemia is reported to be one of the most common side effects of mizoribine (MZR). However, previous clinical trials have not specially focused on MZR-related hyperuricemia. MethodsThirty-nine kidney recipients underwent a switch from mycophenolate mofetil (MMF) to MZR due to adverse clinical events. The control group included 39 kidney recipients continuing MMF without obvious adverse clinical events. They all received cyclosporine (CsA), prednisone, and MMF before enrollment. Every control was matched with a study group patient based on each pair undergoing kidney transplantations during the same week. Over the 24-month follow-up, every recipient underwent a physical examination including blood pressure, and laboratory screening of serum uric acid (sUA), creatinine, albumin, and CsA trough concentrations. We also calculated the estimated glomerular filtration rate (eGFR). ResultsThe sUA level of the study group significantly and consistently increased during the first 5 months, and then decreased. By 18 months, sUA concentrations were not significantly different between the 2 groups (P = .068). There were more new hyperuricemic cases in the study group at 24 months. There were no significant differences in blood pressure, eGFR, and CsA levels between the 2 groups. ConclusionAdministration of MZR was associated with a significant, transient increase in sUA. The increased uric acid suggested that MZR interferes with purine metabolism. The decrease should be associated with hypoxanthine-guanine phosphoribosyl transferase (HGPRT) enzyme activity, which improved under long-term MZR treatment. Therefore, recipients who receive MZR should be monitored more frequently for sUA during the first 5 months, followed by standard monitoring after 18 months.
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