It is well known that patients with gout frequently have acidic urine, a major risk factor for urolithiasis. However, the underlying mechanism of acidic urine in patients with gout remains unclear. Recently, uric acid nephrolithiasis has been reported to be a factor contributing to of renal manifestation of metabolic syndrome. Therefore, to clarify the mechanism of acidic urine in patients with gout, we investigated the relationships between urinary pH and other components of metabolic syndrome. Patients with a 24-hour urinary pH below 5.5 showed higher or greater levels of blood pressure, serum triglyceride, blood sugar, plasma insulin, and visceral fat area, compared with those with a 24-hour urinary pH above 5.5. In addition, there were negative relationships between 24-hour urinary pH and serum triglyceride, visceral fat area, and HOMA index. PPAR a agonist, bezafibrate, significantly raised the 24-hour urinary pH in gout patients in accordance with a reduction in serum triglyceride concentration and HOMA-R, probably through improvement of insulin resistance. These findings suggest that insulin resistance plays at least a partial role in the development of acidic urine in patients with gout.