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After the introduction of cyclosporin, the graft survival rate of renal transplant and patients’’ life expectancy have been greatly improved. However, cyclosporin is known to cause several undesirable side effects, one of which is hyperuricemia, which may subsequently cause gouty nephropathy and graft dysfunction. The purpose of this study was to evaluate the frequency and predisposing factors of hyperuricemia in cyclosporin-treated patients within one year of kidney transplantation and uricosuric efficacy of benzbromarone. The patients who were treated with cyclosporin after kidney transplantation in 1998 and the patients who were treated with benzbromarone for the control of cyclosporin-induced hyperuricemia in 1999 were investigated retrospectively. Among the 76 patients in cyclosporin-treated patients in 1998, hyperuricemia occurred in 55 patients (72.4%) and the mean time from kidney transplantation to occurrence of hyperuicemia was 5.0pm8.0 months. In 1999, 22 patients were treated with benzbromarone for hyperuricemia and their mean time from kidney transplantation to occurrence of hyperuricemia was 4.5pm10.4 months. Acute rejection developed in one patient (4.8%) out of 21 normo-uricemic patients and 11 patients (20.0%) out of 55 hyperuricemic patients in 1998. The difference of rejection rate in these two groups was significant (p<0.001). There was no difference of rejection rate between before and after treatment of benzbromarone. Cyclosporin trough levels did not show a significant correlation with the serum uric acid levels among the three groups. However, hyperuricemic patients showed significantly higher serum creatinine levels than patients with normal uric acid levels (p<0.001). Benzbromarone decreased serum uric acid levels from 8.3pm2.3;mg/dl;to;5.1pm2.0;mg/dl (p<0.0001) and normalizing serum uric acid in all of 22 patients. Except for one patient (4.5%) who experienced diarrhea, no significant side effect was noted.
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