Studies were carried out on multiple urine-samples from eight patients with recurrent idiopathic-calcium oxalate stone formation and eight normal-persons to define an index of the risk of forming-calcium oxalate stones. Under the same conditions of dietary and fluid intake the urine samples of the patients with stone formation were more supersaturated with calcium oxalate (P < 0.001) and had lower concentrations of protective inhibitors of crystallization (P < 0.001) than those of the controls. However, the best separation between the groups was defined by a discriminant line relating inhibitory activity and urine-saturation. A measure of the risk of forming large crystals, the saturation-inhibition index, was defined as the distance of each urine from the discriminant line. The patients with stone formation had a significantly higher-mean saturation-inhibition index than the controls (P < < 0.001). Both the percentage of large calcium oxalate crystals excreted (P < 0.001) and the stone episode rate (P < 0.005) were significantly correlated with the saturation-inhibition index. (N Engl J Med 294:-249-252, 1976). The problem of calcium oxalate stone formation in the urinary tract has perplexed investigators for many centuries. The simplest hypothesis proposes that the first step in stone formation involves the spontaneous precipitation from urine, excessively oversaturated with calcium oxalate, of a crystal or aggregate of crystals large enough to become trapped at some narrow part of the urinary tract. This trapped particle is considered to act as a nidus for the formation of a stone. Indeed, much evidence has accumulated to support the proposition that periods of crystalluria are necessary to trigger off stone formation in animals12and in man.
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