Journal of Clinical Endocrinology & Metabolism, Vol 49, 742-747, Copyright © 1979 by Endocrine Society

ARTICLES

Selective hypoaldosteronism with hyperreninemia in a diabetic patient

S Morimoto, KS Kim, I Yamamoto, K Uchida, R Takeda and L Kornel

A 62-yr-old diabetic woman exhibited low plasma and urinary aldosterone levels in the face of markedly elevated PRA during the course of nonketoacidotic hyperglycemic precoma with dehydration, hyponatremia, and hyperkalemia, for which she was hospitalized. Studies performed after her recovery from precoma revealed hyperreninemic hypoaldosteronism with normal adrenoglucocorticoid function. While the patient was supine, PRA on a 256-meq sodium intake was at or above the upper limit of the normal range for a 200-meq sodium intake; furthermore, after sodium depletion with furosemide and 4 h of ambulation, PRA markedly increased. No increases in plasma inactive renin were found. Plasma renin substrate concentration was normal. Plasma levels and urinary excretion of aldosterone were low and increased slightly during sodium restriction with insulin treatment, accompanied by hyperkalemia and sodium loss, despite markedly elevated PRA. Repository ACTH administration induced sodium retention and potassium loss with a normal increase in urinary 17- hydroxycorticosteroids. Plasma levels of deoxycorticosterone, corticosterone, and 18-hydroxycorticosterone were normal, while plasma aldosterone was low. Levels of these mineralocorticoids remained unchanged during angiotensin II infusion on both 256-meq and 100-meq sodium intakes. Rapid ACTH administration produced normal increases in plasma deoxycorticosterone and corticosterone but caused a subnormal increase in plasma aldosterone. These results suggest adrenal insensitivity to angiotensin II, possibly a defect in adrenal angiotensin II receptors, as the cause of hypoldosteronism with hyperreninemia in this patient.