[A study on the pathogenesis of hyporeninemia in diabetics].

Abstract

Hyporeninemic hypoaldosteronism has mainly been described in patients with diabetes mellitus. In order to elucidate the mechanisms of hyporeninemia in diabetic patients, the author studied the response of active renin concentration (ARC) and inactive renin concentration (IRC) to the administration of captopril or sodium depletion in patients with diabetes mellitus and glomerulonephritis and in normal subjects. The diabetic patients were separated into four groups: Group 0, diabetic patients without neuropathy or nephropathy; Group I, those with neuropathy without nephropathy; Group II, those without neuropathy with nephropathy; Group III, those with neuropathy and nephropathy. Diabetic patients with some complications had slightly lower plasma active renin levels than those without complications. The mean increase in plasma active renin after captopril (delta ARC) and sodium depletion was lower in group I than in group 0, and there was no difference between group II and group 0. There was no correlation between delta ARC and creatinine clearance (Ccr) in diabetes mellitus. Plasma prorenin was higher in group I than in group 0, and there was no difference between group II and group 0. No significant change of prorenin after captopril was observed in all groups, but the mean increase in plasma inactive renin after sodium depletion was slightly higher in groups I and III than in groups 0 and II. ARC/IRC was significantly lower in group I than in group 0, and there was no difference between group II and group 0. There was no correlation between ARC/IRC and Ccr in diabetes mellitus, but significant correlation between ARC/IRC and postural change in systolic blood pressure. In three diabetic patients with hyporeninemic hypoaldosteronism, the postural fall in systolic blood pressure was significant, and ARC/IRC was significantly low, but IRC was not high. These results suggest that autonomic dysfunction is a major factor in an impairment of the processing of prorenin to active renin in diabetic patients, and severe autonomic dysfunction may impair the biosynthesis of prorenin in patients with hyporeninemic hypoaldosteronism.