Abstract

Hyperuricosuria has been considered as a risk factor for calcium stone formation (1) and thought to be mainly a result of consumption of purine rich animal protein (2). According to Coe (3) some hyperuricosuric patients could not decrease their excretion of urate on a low purine diet to the same extent as controls and he suggested that a defect in the renal handling of urate may exist. We have earlier shown (4) that stone formers with a proximal renal tubular acidosis (pRTA) have a higher serum urate than patients with a normal acidification of the urine. Hyperuricemic patients with RTA also have a lower urate excretion than hyperuri cemic patients with a normal acidification of the urine (4). The aim of the present study was to investigate if hyperuricosuria or renal acidification defects in calcium stone disease were associated with a dysfunction in the renal tubular handling of urate. Furthermore, the object was to find out to what extent serum and urinary urate could be explained in terms of renal tubular transport phenomena.

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