Hyperaldosteronism is associated with elevated cardiovascular risk. Using
mineralocorticoid receptor antagonists a significant reduction in mortality was archived in patients with
heart failure. In addition, in refractory
hypertension and in patients with
metabolic syndrome aldosterone seems to play an important role.
Therapy with mineralocorticoidreceptor (MR) antagonists is feasible when
aldosterone levels are elevated, in particular in patients with
aldosterone-escape. Of particular interest is primary
aldosteronism (PA). PA is one of the major causes of secondary
hypertension. Since most patients with PA present with normokalemia screening has to be performed using the
aldosterone renin ratio, in particular patients with refractory
hypertension, young hypertensive patients and patients with incidentaloma. One has to point out that drugs that interfere with the
aldosterone-
renin-
aldosterone-system need to be discontinued or changed. After successful screening, confirmatory testing (e.g. i.v.
salt suppression test) has to follow. In order to differentiate between unilateral and bilateral disease computed tomography and adrenal vein sampling are performed. While unilateral
adenomas can be cured surgically, bilateral adrenal
hyperplasia is treated with MR-antagonists. In case of positive family history for PA one should consider familiar
hyperaldosteronism (FH). Three forms are currently defined--FH type I, type II and type III. A hybrid gene consisting of
CYP11B1 and
CYP11B2 that produces
aldosterone in an
ACTH dependant manner can be found in FH type I. Diagnosis is verified by long range PCR. No underlying monogenetic cause for FH II and FH II could be detected so far. Through mechanisms way more than water and
salt regulation,
hyperaldosteronism can negatively influence cardiovascular mortality and morbidity and should therefore play an important part in diagnosis and
therapy of arterial
hypertension.