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Perspectives PAPA

Arterial hypertension is a major cardiovascular risk factor that affects between 10-40% of the population. Primary aldosteronism due to adrenal excess production of aldosterone is the most common curable form of hypertension affecting 4-12% of hypertensives. Given the severe cardiovascular adverse effects of aldosterone excess early detection and individualized treatment of primary aldosteronism has an important impact on clinical outcome and survival. However, the pathophysiology of primary aldosteronism is not well understood: While we recently identified specific genes underlying aldosterone producing adenoma, the most prevalent form of primary aldosteronism, bilateral adrenal hyperplasia, has remained enigmatic. It is the hypothesis of this ERC proposal that the pathophysiology of primary aldosteronism is a process based on two ‘hits’: agonistic angiotensin II type 1 receptor (AT1R) autoantibodies and somatic mutations. Whereas agonistic autoantibodies induce proliferation and grossly changes adrenal cortex architecture towards diffuse or nodular hyperplasia, somatic mutations result in adenoma formation. Taken together, both factors induce not only aldosterone but also marked glucocorticoid excess.

Interview with Prof. Reincke on the aims of ERC PAPA



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