Increased Plasma Aldosterone in Patients with Clinical Depression

Background al depression has been increasingly recognized as an independent risk factor for adverse cardiovascular events, but the biological mechanisms of this association remain unclear. Recent evidence for renin system dysregulation in patients with depression led us to hypothesize that aldosterone—a well-recognized contributor to vascular injury—could be increased in depressed patients. The present study was designed, therefore, to be a cross-sectional investigation of plasma renin and aldosterone levels in depressed patients as compared with healthy controls with no history of psychiatric illness. s l of 65 depressed patients and 65 age- and gender-matched control subjects were enrolled. Following a fixed sodium and potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the influence of circadian rhythms. s gh there were no significant differences in plasma level of renin among subjects with depression and controls (7.9 ± 5.8 vs. 6.4 ± 4.3 pg/mL, respectively; p = 0.10), depressed subjects exhibited greater mean aldosterone levels as compared with control subjects (157.2 ± 67.5 vs. 125.7 ± 38.1 pg/mL, respectively; p = 0.0014). After adjusting for potential confounders, multivariate logistic regression analysis showed that subjects with depression had 2.77 times higher odds of elevated aldosterone levels compared with healthy control subjects (95% confidence interval, 1.30–5.92, p = 0.008). sions esent findings support the hypothesis that hyperaldosteronism could be a common feature among depressed patients, thereby suggesting that increased aldosterone levels may act as a mediator in the pathway linking depression to unfavorable vascular events.