Profibrotische effecten van aldosteron

- 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 11β-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.