Uric acid nephrolithiasis is typically found in individuals with a low urine pH and a normal concentration of urinary uric acid. Patients with a history of gout are at greater risk of forming uric acid stones, as are patients with obesity, diabetes or the complete metabolic syndrome. The unifying renal tubular abnormality of these disorders appears to be the excretion of 1 abnormally acidic urine. Gout is an inflammatory disease characterized by hyperuricemia that leads to acute arthritis with monosodium urate crystal deposition and is associated with 1 uric acid kidney stones. The association between gout and an increased prevalance of uric acid stones appears logical. Clinically gout is caused by an elevated level of serum uric acid that leads to deposition of crystals in the joints and tissues, and intuitively an increase in uric acid excretion. However, this paradigm is not consistent with the observation that approximately 90% of patients with hyperuricemia and gout have a defect in uric acid excretion. Patients with gout form kidney stones due to a persistently low urinary pH, which favours formation of the relatively insoluble 1 uric acid rather than the more soluble urate. Excessively acidic urine is found in patients with complete metabolic syndrome, as well as those with only type 2 diabetes and/or obesity. Renal tubular insulin resistance has been implicated as a causative 1 factor in excretion of overly acidic urine.