Primary Hyperaldosteronism: NP Mgmt

Primary hyperaldosteronism (PA, Conn syndrome) is autonomous aldosterone production independent of the renin-angiotensin system. Aldosterone, produced by the zona glomerulosa, acts on the mineralocorticoid receptor (MR) in the renal collecting duct principal cells, upregulating ENaC (epithelial sodium channels) and ROMK (potassium channels). This causes sodium reabsorption (leading to volume expansion and hypertension) and potassium/hydrogen ion excretion (causing hypokalemia and metabolic alkalosis). The volume expansion suppresses renin via the juxtaglomerular apparatus, creating the hallmark biochemical signature: elevated aldosterone with suppressed renin (elevated aldosterone-to-renin ratio). PA accounts for 5-13% of hypertension cases and is the most common cause of secondary hypertension. Importantly, aldosterone causes cardiovascular damage BEYOND its hemodynamic effects: MR activation in cardiac and vascular tissue promotes fibrosis, inflammation, endothelial dysfunction, and oxidative stress, leading to LVH, atrial fibrillation, stroke, and MI at rates exceeding those of matched essential hypertension.