EFFECT OF URIC-ACID ON PLASMA-LEVELS OF 1,25(OH)2D IN RENAL-FAILURE

Previous studies from these laboratories have demonstrated that uremic biologic fluids contain substances that suppress 1,25(OH)2D metabolis m. Among these substances, it was found that uric acid suppresses 1alp ha-hydroxylase activity and synthesis of 1,25(OH)2D in rats. In this s tudy, the effect of uric acid on plasma concentrations of 1,25(OH)2D i n patients with renal failure was examined. Nine patients with stable chronic renal failure (serum creatinine, 1.9 to 6.4 mg/dL) were studie d. None of the patients received vitamin D supplementation. Plasma con centrations of Ca, P, parathyroid hormone, creatinine, uric acid, 1,25 (OH)2D, and 25(OH)D were measured before and 1 wk after the patients r eceived allopurinol, 300 mg daily. Plasma creatinine, Ca, P, parathyro id hormone, and 25(OH)D did not change before or after allopurinol tre atment. However, plasma uric acid decreased significantly from 7.3 +/- 0.4 to 4.0 +/- 0.4 mg/dL (P < 0.01) and plasma concentration of 1,25( OH)2D rose from 30.8 +/- 2.7 to 38.2 +/- 4.8 pg/mL (P < 0.01) after th e ingestion of allopurinol. Allopurinol itself did not appear to direc tly enhance 1alpha-hydroxylase activity in rats. It was concluded that a short-term administration of allopurinol suppresses plasmic uric ac id and increases plasma 1,25(OH)2D in patients with chronic mild to mo derate renal failure.