The ability of insulin to stimulate glucose disposal by muscle varies widely within the population at large. Individuals with muscle insulin resistance develop type 2 diabetes if they cannot compensate for this defect by secreting large amounts of insulin. Although this philanthropic effort on the part of the pancreatic B-cell may prevent gross decompensation of glucose homeostasis, it renders such individuals at increased risk to develop a cluster of abnormalities (syndrome X) associated with coronary heart disease. Although the kidney is not considered to be an insulin sensitive tissue, two features of syndrome X, hyperuricemia and hypertension, are likely to be dependent on the retention of normal insulin action on the kidney. More specifically, there is evidence to support the hypothesis that elevated plasma insulin concentrations may enhance renal sodium retention and decrease urinary uric acid clearance. As such, it is possible that a normal kidney response to the compensatory hyperinsulinemia associated with insulin resistance in nondiabetic subjects contributes to the development of hyperuricemia and hypertension in such individuals.