Uric acid nephrolithiasis comprises 8-10% of patients with kidney stone disease. However, this prevalence is higher in particular ethnic populations and in certain regions of the world. The major pathophysiologic mechanism for uric acid nephrolithiasis is unduly acidic urine. At a urinary pH below 5.5, the concentration of sparingly soluble uric acid increases and promotes the formation of uric acid stones. Unduly acidic urine is likely due to defective renal ammoniagenesis. Moreover, emerging studies suggest that increased endogenous acid production, in addition to defective urinary ammonium buffering, may also be responsible for the abnormally acidic urine in this population. The underlying mechanism of low urinary ammonium and increased endogenous acid production has been linked to the metabolic syndrome and may also be associated with renal fat accumulation in the kidney. Although low urinary pH is necessary, it alone is not sufficient for uric acid crystal precipitation. This implies the potential role of inhibitors and/or promoters of uric acid crystallization.
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