ABSTRACT

Peripheral resistance to the action of insulin occurs in almost all uremic subjects and is largely responsible for the abnormal glucose metabolism seen in this setting (2-4). Impaired tissue sensitivity to insulin has already been demonstrated in patients with only mild to moderate reductions in renal function (5). Both experimental and clinical studies suggest that skeletal muscle is the primary site of insulin resistance (2,3), presumably due to a postreceptor defect (6,7).