Hyperreninemic Hypoaldosteronism in the Critically 111: A New Entity*

TLDR

The study aims to define changes in adrenal gland function during critical illness. The authors evaluated 28 severely ill patients with persistent hypotension admitted to a medical ICU. Patients showed hypercortisolemia, markedly elevated renin, and selective hypoaldosteronism despite normal potassium, with a 78 % mortality rate among those with low aldosterone, indicating a new entity of hyperreninemic hypoaldosteronism in critically ill hypotensive patients.

Abstract

To define the changes in adrenal gland function during critical illness, we evaluated 28 severely ill patients with ersistent hypotension who were hospitalized in a medical intensive care unit. The patients had increased plasma cortisol (mean ± SE, 40.1 ± 10.1 jug/dl). PRA was increased in all subjects (21.6 ± 7.2 ng/ml'h); however, the plasma aldosterone concentration was inappropriately low in 18 of the subjects, with values ranging from 1-9 ng//dl, despite normal serum potassium concentrations (4.3 ±0.1 meq/liter) and increased concentrations of the aldosterone percursor, 18-hydroxycorticosterone. These 18 patients had hypotension associated with major infections and a high mortality rate (78%). Infusions of ACTHor angiotensin II were associated with a normal aldosterone response in only 2 of the 14 patients tested, also suggesting that the defect was probably at the level of the zona glomerulosa cell. Although infection was a common underlying illness, no other factors, such as dopamine administration, decreased angiotensin-converting enzyme activity, or increased aldosterone clearance, could be implicated as the cause of the phenomena. Thus, selective hypoaldosteronism in the presence of high renin levels exists in a substantial percentage of hypotensive critically ill patients.(J Clin Endocrinol Metab53: 867, 1981)