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.