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Renal stone disease (nephrolithiasis) is a relatively common problem [1,2]. Older studies estimated that 12 percent of men and 5 percent of women will have at least one symptomatic stone by the age of 70 [1].
In a report from the third National Health and Nutrition Examination Survey, the population prevalence increased from 3.8 percent in the period 1976 to 1980 to 5.2 percent in the years 1988 to 1994 [2]. The prevalence increased in men and women, and whites and blacks. However, the incidence rates since then may have leveled off [3].
Approximately 75 percent of patients with nephrolithiasis form calcium stones, most of which are composed primarily of calcium oxalate or, less often, calcium phosphate [1,4]. Pure uric acid stones make up less than 10 percent of all stones.
This topic provides an overview of the pathogenesis and risk factors for calcium nephrolithiasis. The evaluation and management of the patient with kidney stones, prevention of recurrent calcium stones, and related topics are discussed separately. (See "Diagnosis and acute management of suspected nephrolithiasis in adults" and "Evaluation of the adult patient with established nephrolithiasis and treatment if stone composition is unknown" and "Prevention of recurrent calcium stones in adults".)
Stones are more likely to occur when one or more factors are present that lead sequentially to supersaturation of the urine, the formation of crystals, and their subsequent aggregation into a clinically detectable stone. Even individuals without nephrolithiasis can excrete crystals; however, calcium oxalate stone formers are more likely to have crystalluria than controls, and the presence of crystalluria substantially increases the likelihood of stone formation (picture 1A-B) [5].
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