Renal Handling of Uric Acid in Gout by Means of the Pyrazinamide and Probenecid Tests

Abstract

The protagonism of the kidney in the pathogenesis of primary gout is essential because at least three-fourths of all patients have normal urate production and require an elevated plasma urate concentration to obtain a normal uric acid excretion^1,2. Recent investigations of the urate transport system in the human kidney have provided evidence for a 4-component model: glomerular filtration, proximal or presecretory reabsorption, tubular secretion, and postsecretory reabsorption³. According to this model, renal hypouricemia might result from diminished glomerular filtration rate (GFR), augmented either presecretory or postsecretory reabsorption, or diminished tubular secretion of uric acid. In an attempt to determine the site of the renal abnormality resulting in decreased clearance of urate, we examined the tubular phases that govern uric acid excretion in a gouty population in the states of hyperuricemia and hypouricemia.