[Profibrotic effects of aldosterone].

Animal studies have shown that during high sodium intake aldosterone induces cardiac fibrosis and renal nephrosclerosis through activation of mineralocorticoid receptors. In the human heart mineralocorticoid receptors and activity of the enzyme 11beta-hydroxysteroid-dehydrogenase type 2, which is required for the activation of mineralocorticoid receptors by aldosterone, are both present. In clinical medicine the profibrotic effect of aldosterone has been related to diastolic dysfunction, arrhythmia and progression of cardiac and renal failure. The addition of an aldosterone receptor antagonist to optimal treatment in patients with heart failure causes a decrease in serum markers of collagen turnover and a decline in cardiac morbidity and mortality. These findings are a strong indication of a profibrotic effect of aldosterone in cardiac failure. Studies concerning the profibrotic effect of aldosterone in patients with primary hyperaldosteronism are contradictory and at the moment no data are available about a potential antifibrotic effect of aldosterone receptor antagonists in patients with impaired renal function.