1985 Volume 27 Issue 11 Pages 1599-1604
Suppressed plasma aldosterone concentration (p-Ald) in relation to plasma renin activity (PRA), termed as hyperreninemic hypoaldosteronism (HH), has been shown to occure in some patients with critically ill patients. We investigated the incidence of this new entitiy of HH in 32 patients (19%). None of these HH patients presented with symptoms related to hypoaldosteronism, such as hyperkalemia or metabolic acidosis. There were no significant difference in serum sodium, potassium and creatinine levels between the hypotensive (n=8) and normotensive (n=24) groups of overall critically ill patients. Arterial blood oxygen tension were slightly lower but not significantly different in both groups. p-Ald and 18-OH corticosterone (18-OHB), the aldosteone precursor were slighty lower, and PRA and p-Aid/PRA ratio were somewhatlower in hypotensive group. However, there were no significant differences in any of these parameters. Plasma cortisol was significantly higher in hypotensive group (p<0.05), suggesting much potent stress in this group. When all the patients were subclassified into high PRA (PRA more than 3.0 ng/ml/h) and normal or low PRA according to the basal PRA levels, p-Ald and p-Ald/PRA ratio were significantly lower (p<0.05) in hypotensive group. In three of six patients who developed HH, episode of hypotension was noted, while in the remaining three patients hypotension was not evident. From these results, it is concluded that HH may not be a rare complication of critically ill patients. However, symptomatic HH is infrequent, suggesting HH is either imcomplete or transient. A possible site of impairment in aldosterone biosynthesis might be both in early and late steps of synthesis. The etiology of HH in critically ill may not be explained solely by hypoperf usion of adrenal glomerulosa, since there appeared to be no significant linkage between known duration or severity of hypotension and the development of HH the present series.
