DIABETIC SODIUM RETENTION - THE PATHOPHYSIOLOGICAL ROLE OF HUMAN ATRIAL-NATRIURETIC-PEPTIDE IN PATIENTS WITH DIABETES-MELLITUS

Diabetic sodium retention, the previously demonstrated increase in exchangeable body sodium in patients with diabetes mellitus by approximately 10% in comparison to nondiabetic subjects, is again finding broad clinical interest evoked by the current discussion on hyperinsulinemia and metabolic syndrome in hypertensive patients. Diabetic sodium retention, however, is a consequence of impaired glucose homeostasis and not mainly an insulin-induced phenomenon. Due to long-standing hyperglycemia resulting from stable but insufficient metabolic control, there is an impairment of the natriuretic responsiveness to various natriuretic stimuli, among these human atrial natriuretic peptide (hANP), the most potent endogenous natriuretic principle known at present. Whereas diabetic sodium retention may act as pacemaker for the development of hypertension and, possibly, kidney disease in diabetic patients, hANP, apart from its blunted natriuretic efficacy, is apparently not involved into the pathogenesis of these sequelae of diabetes mellitus.