Abstract

I
UA stone comprises 8%–10% of all kidney stones in the United States, especially in patients with metabolic syndrome (type 2 DM and obesity). 2 Duvdevani et al. reported a higher incidence of UA stones in patients with diabetes (41%). 3 Insulin resistance type 2 DM results in lower urine pH through impaired ammonium excretion. A low urine pH plays a major role of UA stone formation.
To date, previous studies have identified that DM may be associated with higher risk for nephrolithiasis. 1,2 The increasing prevalence of kidney stones, as well as the burden of stone disease on society, is enormous. Therefore, understanding the pathophysiologic underpinnings of urolithiasis formation will contribute to establish a more rational and economical approach for nephrolithiasis management, with greater emphasis on stone prevention being imperative rather than symptomatic treatment. The correction of impaired glucose tolerance could obviously reduce kidney stone risk. 4
