Metabolic syndrome and the genesis of uric acid stones

Abstract

Uric acid stones are significantly more common among nephrolithiasis patients with type 2 diabetes, obesity, and/or the metabolic syndrome. The principal metabolic feature responsible for this association is an overly acidic urine, which leads to the precipitation of sparingly soluble uric acid crystals in urine and subsequent development of stones. The unduly acidic urine in uric acid stone formers is caused by a combination of excessive dietary intake of animal proteins and a defect in renal ammoniagenesis and/or excretion that leads to impaired buffering and amplifies the acidic urine caused by an increased acid excretion.

Figure 1. Relationship between 24-hr urine pH and 24-hr urine sulfate (a marker of dietary animal protein intake) in subjects with (□) and without (■) the metabolic syndrome

Data from 148 non-stone forming volunteers. Subjects with the metabolic syndrome exhibited a significantly higher 24-hr urine sulfate, indicating greater consumption of acidogenic diet. The regression line for each group shows that 24-hr urine pH declines with increasing acid intake (24-hr urine sulfate). However, at any given 24-hr urine sulfate, 24-hr urine pH is significantly lower in subjects with the metabolic syndrome, suggesting that factors besides dietary acid intake contribute to the more acidic urine.