Abstract
The factors which play a determinant role in urinary stone formation can be broadly classified into two main categories — those affecting the supersaturation of the urine with respect to the precipitating salt, and those which influence the ability of the urine to inhibit crystal nucleation, growth and aggregation. The supersaturation of urine with calcium oxalate is principally a function of calcium and oxalate excretion1 and urinary pH, while inhibitory activity has been attributed to the presence of pyrophosphate and glycosaminoglycans (GAGS)2. For some years uric acid has been implicated in calcium oxalate stone formation3 by virtue of its effect on calcium oxalate solubility4 and the capability of its sodium salt of inducing heterogeneous nucleation of calcium oxalate. More recently2 it has been proposed that uric acid can indirectly predispose to calcium oxalate stone formation by interacting with urinary GAGS, thereby reducing their inhibitory capacity. Although it is widely accepted that urine can strongly inhibit crystal growth and aggregation, the significant reduction6 of this activity in urine from stone-formers compared with normal subjects has not been confirmed7.
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