Abstract
A group of patients forming calcium oxalate stones are hyperuricosuric and it is thought that their excessive urate excretion contributes to calcium-stones formation1. The pathomechanisms invoked are dietary purine excess and endogenous uric acid overproduction, being defective tubular reabsorption of urate “unattractive” because uricemia was found to be normal in patients with recurrent calcium nephrolithiasis (RCN) and hyperuricosuria. Current studies were undertaken to define the incidence, role of diet, abnormalities of the renal handling of urate, and associated metabolic disturbances in patients with RCN and hyperuricosuria.
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