Primary aldosteronism has been considered a rare disease in the past years, affecting 1% of the hypertensive population. Subsequently, growing evidence of its higher prevalence is present in literature, although the estimates of disease range from 5 up to 20%, as in type 2 diabetes and resistant hypertension. The main reasons for these variations are associated with the selection of patients and diagnostic procedures. If we consider that hypertension is present in about 20% of the adult population, primary aldosteronism can no longer be considered a rare disease. Patients with primary aldosteronism have a high incidence of cardiovascular, cerebrovascular and kidney complications. The identification of these patients has therefore a practical value on therapy, and to control morbidities derived from vascular damage. The ability to identify the prevalence of a disease depends on the number of subjects studied and the methods of investigation. Epidemiological studies are affected by these two problems: there is not consensus on patients who need to be investigated, although testing is recommended in subjects with resistant hypertension and diabetes. The question of how to determine aldosterone and renin levels is open, particularly if pharmacological wash-out is difficult to perform because of inadequate blood pressure control. 1. Introduction The history of primary aldosteronism (PA) is that of an uncommon cause of hypertension until up to 15 years ago. In 1954, Conn studied a 34-year-old female with high blood pressure, severe hypokalemia, and mild hypernatremia, discovering an averaged 22-fold higher mineralcorticoid activity per day in comparison with normotensive controls: this clinical condition reversed after the removal of a right adrenal mass. Thereafter, Conn stated in his presidential address “It is believed that these studies delineate a new clinical syndrome which is designated as primary aldosteronism.” Primary aldosteronism, as defined by Conn in 1955 [1], was widely thought to be present in approximately 1% of hypertensive patients [2, 3]. Today primary aldosteronism can be defined as a group of different disorders (Table 1), “in which aldosterone production is inappropriately high, relatively autonomous from the renin-angiotensin system, and non suppressible by sodium loading” [4]. Several studies suggest that PA is the most common cause of secondary hypertension, although the prevalence is variable from 5 to 20%, depending on patient selection and methods of diagnosis. There are changes in the perceived epidemiology of the disease because
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