The uricosuric response to 80 mg of micronized Benzbromarone was employed to assess the renal tubular secretory site for uric acid in patients with primary gout. Since Benzbromarone selectively inhibits tubular reabsorption of secreted urate, the maximum uricosuria induced by this drug can be equated with the minimal secretory rate. Furthermore, a significant relationship was noted in normal controls between urate secretion and the plasma urate concentration (r = 0.956, p less than 0.005). Using the Benzbromarone response as a measure of tubular secretion, gouty patients with normal production hyperuricemia had a significantly lower secretory rate by comparison to patients with overproduction of uric acid. These data indicate that in patients with primary normal production hyperuricemia, the renal tubular defect is related to a decreased secretory response for a given plasma concentration of uric acid.