Aldosterone and the kidney.

The mineralocorticoid aldosterone is a key regulator of blood pressure, fluid and electrolyte homeostasis, and acts via the mineralocorticoid receptor (MR). In recent years, an increasing number of studies revealed deleterious effects of aldosterone via its receptor. Especially in patients with primary hyperaldosteronism (PHA) a significant higher risk of developing cardiovascular comorbidities and comortalities was reported. Also renal insufficiency is clearly increased in patients with PHA indicating a role of aldosterone and the MR in the pathogenesis of renal injury. It has been shown that aldosterone in combination with an elevated salt intake, leads to renal inflammation, fibrosis, podocyte injury, and mesangial cell proliferation. This review focuses on the current knowledge of aldosterone effects in the kidney and highlights this topic from 2 perspectives: from clinical medicine and from experimental studies.

Comorbidities in primary aldosteronism.

Patients presenting with primary aldosteronism experience more cardiovascular events than patients with essential hypertension independent of blood pressure. Therefore, the presence of primary aldosteronism should be detected, not only to determine the cause of hypertension, but also to prevent such complications. This review focuses on human data regarding increased end-organ damage and comorbidities in primary aldosteronism. Special emphasis is put on the effects of aldosterone excess on blood vessels, the heart, the kidney, and the brain. The data reviewed in our article demonstrate that primary aldosteronism is associated with a prevalence of cerebro-, cardiovascular and renal complications that are out of proportion to the blood pressure and benefits substantially from treatment in the long term. In this view, adrenalectomy and aldosterone antagonist treatment seem to be of considerable therapeutic value to control and limit the progression of comorbidities in primary aldosteronism.