Hyperuricemia in Living Donor Kidney Transplantation Patients During Mizoribine Administration Caused Mainly by Changes in Kidney Function

Abstract

BackgroundAlthough mizoribine (MZR) is used as an immunosuppressant after renal transplantation, the occurrence of hyperuricemia has been reported. The onset of hyperuricemia is often observed within the first several months after surgery. Since MZR is a renal excretion-type drug excreted as an unchanged drug from the kidneys, MZR blood concentrations may rise due to the influence of renal function. We investigated whether the onset of hyperuricemia after MZR administration was associated with the direct effect of a change in renal function. MethodsSerum uric acid (serum UA), serum creatinine (sCr), serum β2-microglobulin (serum β2-MG), and serum cystatin C (serum Cys-C) were measured for about 3 months in 22 subjects. Correlation coefficients were calculated using the change rates of serum UA and sCr (Δ serum UA, Δ sCr), serum UA and serum β2-MG (Δ serum UA, Δ serum β2-MG), and serum UA and serum Cys-C (Δ serum UA, Δ serum Cys-C) at the onset of hyperuricemia. ResultsThe correlation coefficients between Δ serum UA and Δ sCr, Δ serum UA and Δ serum β2-MG, and Δ serum UA and Δ serum Cys-C were 0.723 (P < .001), 0.863 (P < .001) and 0.548 (P < .001), respectively. Further, serum UA and sCr level reached their highest peak on the same day after MZR administration, and the behavior was mostly consistent. ConclusionIt was suggested that hyperuricemia occurred about 3 months after MZR administration due mainly to temporary changes in kidney function.