Abstract: Objective? To investigate the clinical characteristics and pathogenesis of hyperuricemia and acute kidney injury (AKI) induced by mizoribine (MZR). Methods? The clinical data of a case of IgA nephropathy with hyperuricemia induced by oral administration of MZR was retrospectively reviewed. Results? A 13 -year-old boy with IgA nephropathy was diagnosed for 5 months. The basic renal function was normal. Transient hyperuricemia and acute renal injury were found after combined use of benazepril and MZR. The uric acid clearance rate (UACl) was significantly reduced to 3.66 mL·min-1 ·1.73 m-2 , the fractional excretion of sodium (FENa) was less than one ( 0. 4%), and the fractional excretion of uric acid (FEUA) was increased to 17 . 1%, highly suggestive of pre-renal AKI. After stopping the above drugs, he received hydration treatment, then the renal function recovered rapidly. Conclusion? Hyperuricemia induced by MZR can not only cause post-renal AKI, but also reduce renal perfusion. When combined with angiotensin converting enzyme inhibitor, the effect of MZR on uric acid metabolism and the adverse reactions should be found in time for further adjustment of the medication.

Key words: ? mizoribine;? angiotensin converting enzyme inhibitor;? hyperuricemia;? acute kidney injury