Abstract
To determine whether an impaired tubular transport mechanism for urate could differentiate the pathogenesis of gouty hyperuricemia and if serum urate influences the renal handling of uric acid, we conducted metabolic studies in 56 patients with primary gout. Tubular reabsorption of urate was normal. Tubular secretory rate was 29.3 ± 8.7 percent of filtered urate as compared to 42.4 ± 4.3 percent in 10 normal subjects for a similar urate filtered load (P < 0.01). Among 30 patients examined in the basal state and at pharmacologically reduced serum urate levels, 24 showed a diminished and 6 normal tubular urate secretion in both states of uricemia. According to the probenecid test, 45 patients evidenced a diminished uricosuric response and 11 normal urate excretion rates. This classification was similar to that obtained by the 24-h urinary urate excretion and was identical to that established by means of [2-14C]uric acid in 8 selected patients. We conclude that an impaired tubular secretion of urate may differentiate gouty underexcretors from uric acid overproducers. Increased serum urate is not the cause but a consequence of the impaired tubular urate secretory mechanism in gout.
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