Primary Aldosteronism (Conn Syndrome)

Primary aldosteronism (PA), often called Conn syndrome, is autonomous aldosterone secretion that continues despite suppression of the renin-angiotensin system. The usual sources are bilateral adrenal disease or a unilateral aldosterone-producing adenoma. Aldosterone activates mineralocorticoid receptors in the renal collecting duct. Sodium and water are retained, expanding extracellular volume and raising blood pressure; potassium and hydrogen ions are excreted, which can produce hypokalemia and metabolic alkalosis. The expanded volume suppresses renin, so the characteristic biochemical pattern is aldosterone that is inappropriately high for a very low renin level. Do not wait for hypokalemia before considering PA. Most affected patients are normokalemic, particularly earlier in the disease or when another medication is altering potassium balance. Persistent aldosterone excess also promotes atrial fibrillation, stroke, myocardial infarction, left-ventricular hypertrophy, and chronic kidney disease beyond the risk expected from blood pressure alone. That extra organ injury is why PA-specific treatment matters even when hypertension appears manageable.