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[Fifty years of subclinical primary aldosteronism: importance of early diagnosis].

Clinical presentation of excessive aldosterone secretion is often not specific. The presence of resistant severe hypertension (HT) and signs of hypokalemia is useful but inconsistent characteristic. Plasma aldosterone level in primary aldosteronism (PA) could be normal, although inappropriately high for a low plasma renin activity and not suppressed by sodium. Screening of hypertensive population with no obvious signs of PA has revealed an increased prevalence of idiopathic adrenal hyperplasia as a cause of aldosterone excess. Nowadays, PA is the most common endocrine form of secondary HT, with an estimated prevalence 5-10% of hypertensive population. The diagnosis of PA can lead to surgical cure in the case of aldosterone producing adenoma and unilateral adrenal hyperplasia. The aldosterone excess is responsible for vascular inflammation and end-organ damage. Left ventricular hypertrophy, cardiac arrhythmia and cerebral insult are frequently seen in PA and preventable by mineralocorticoid receptor blockers. For this reason, screening for PA in patients with HT and hypokalemia and/or adrenal incidentaloma, resistant and severe HT, and in patients with the onset of HT at young age is advisable.The most widely accepted screening for PA is serum aldosterone to plasma rennin activity (aldosterone: PRA) ratio, with the cut-off of 30 ng/dl:ng/ml/h. Serum aldosterone level could be included as an additional screening parameter. Confirmatory tests are crucial for the diagnosis of PA in patients with an increased aldosterone: PRA ratio and subtype differentiation for the choice of treatment.