Hyperreninemic Hypoaldosteronism in the Critically 111: A New Entity*

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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)