Abstract

Primary aldosteronism (PA), a significant and curable cause of secondary hypertension, occurs in 5—10% of hypertensive patients, with prevalence dependent on the severity of hypertension. The main etiologies of PA include bilateral idiopathic hypertrophy (BIH) and aldosterone‑producing adenoma (APA), while less common causes include unilateral hyperplasia, familial hyperaldosteronism (FH) types I—IV, aldosterone‑producing carcinoma, and ectopic aldosterone synthesis. This condition, characterized by excessive secretion of aldosterone, leads to increased reabsorption of sodium and water along with potassium loss, culminating in the distinct clinical signs of elevated aldosterone, suppressed renin, and hypertension. It should be noted that hypokalemia is present in only 28% of patients with PA and is not the main indicator. The association of PA with an increased risk profile for cardiovascular disease, regardless of blood pressure level, is notable. Patients with PA show an increased rate of cardiovascular events compared to patients with essential hypertension, adjusted for age, sex, and blood pressure level. Despite its prevalence, PA often remains undiagnosed, highlighting the need for enhanced screening protocols. The diagnostic process for PA involves a three‑pronged assessment: the aldosterone/renin ratio (ARR) as the initial screening tool, followed by confirmatory and subtype tests. A positive ARR requires confirmatory testing to rule out false positives. Examination to detect PA should be carried out in patients with arterial hypertension: moderate (> 160—179/100—109 mm Hg) or severe (> 180/110 mm Hg); resistant to treatment; with idiopathic or diuretic‑induced hypokalemia; with an accidentally diagnosed tumor of the adrenal glands; if first‑generation relatives are diagnosed with PA, or family history indicates early onset of arterial hypertension, or cerebrovascular disorders at a young age (< 40 years); with accompanying obstructive sleep apnea.

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