In fact, since its discovery in 1954 the term primary has been used to emphasize our ignorance of its causes. PA can mimic primary (essential) hypertension, and is still perceived as an exceptionally rare condition necessitating a complex diagnostic workup, given the lack of known mechanisms and therefore of specific biomarkers. Primary aldosteronism (PA) occurs in 5% to 20% of hypertensive patients ( 9, 10) but is often overlooked because patients are not screened for it. This indicates that aldosterone produced in excess with respect to sodium status is a main determinant of high blood pressure, but it is clear from clinical studies from around the world that inappropriately high aldosterone concentrations produce prominent target organ damage, thus contributing to an ominous prognosis ( 4–8). However, aldosterone levels are inappropriately high in 50% to 80% of all hypertensive disorders, not only primary and secondary aldosteronism but also overweight and obesity ( 1, 2) and the most severe (stage II to III) or drug-resistant forms of hypertension ( 3). Clinical aspects, such as epidemiology and diagnosis of primary aldosteronism (PA), are briefly reviewed, and the potential role of circulating and tissue biomarkers of APA in subtyping PA is discussedĪldosterone, the main mineralocorticoid hormone, is vital for maintaining body fluid and electrolyte homeostasis, vascular resistance, and, thereby, blood pressure under conditions of salt/water (volume) depletion.
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