NATURAL-HISTORY AND ETIOLOGY OF HYPERURICEMIA FOLLOWING PEDIATRIC RENAL-TRANSPLANTATION

A retrospective review was conducted to determine the incidence, etiol ogy, natural history and complications of hyperuricemia after pediatri c renal transplantation. Of 81 active transplant recipients aged 10.1 +/- 4.8 (mean +/- SD) years being followed by St. Christopher's Hospit al for Children, 57 (70%) were males and 59 (73%) Caucasian. Their imm unosuppression consisted of azathioprine, cyclosporine A and prednison e. Mean serum uric acid concentrations peaked at 6 months post transpl antation (6.2 +/- 2.6 mg/dl), when 39% of the patients had hyperuricem ia and 60% were receiving diuretics, and decreased thereafter. At 30 m onths, 23% of the patients had hyperuricemia and 17% required diuretic s. When we compared 42 normouricemic (group A) with 24 hyperuricemic ( group B) patients at 18 months post transplantation, we found that pat ients in group B were older (11.6 +/- 4.2 vs. 8.6 +/- 5.2 years, P = 0 .01), had worse renal function (77 +/- 25 vs. 96 +/- 36 ml/min per 1.7 3 m(2), P = 0.03) and required diuretics more frequently (63% vs. 21%, P = 0.001), but had identical blood levels of cyclosporine A (82 +/- 28 vs. 84 +/- 35 ng/ml, P = 0.78). A family history of gout did not af fect the prevalence of hyperuricemia after transplantation. Asymptomat ic hyperuricemia is common following pediatric renal transplantation a nd is more likely attributable to reduced renal function and diuretic therapy than to the known hyperuricemic effect of cyclosporine A. Of t hese variables, only diuretic therapy is readily controllable and shou ld be closely regulated following pediatric renal transplantation.