Conn syndrome

Conn syndrome results from autonomous aldosterone overproduction by the adrenal zona glomerulosa, most often due to a unilateral aldosterone-secreting adenoma (Conn's original description) or bilateral idiopathic adrenal hyperplasia (more common overall). Excess aldosterone acts on the principal cells of the renal collecting duct, increasing Na+ reabsorption (via ENaC) and K+/H+ excretion, leading to hypertension, hypokalemia, and metabolic alkalosis. Because aldosterone is elevated independent of renin, plasma renin activity is suppressed, resulting in a high aldosterone-to-renin ratio (ARR), which is the key screening test. Patients often present with resistant/refractory hypertension, muscle weakness, cramps, and polyuria (from hypokalemia-induced nephrogenic diabetes insipidus); some patients may be normokalemic. Diagnostic workup: screen with plasma aldosterone/renin ratio; confirm with saline suppression, captopril challenge, or oral sodium loading test showing failure to suppress aldosterone; then use adrenal CT and adrenal vein sampling to localize unilateral vs bilateral disease. Treatment: unilateral adenoma → laparoscopic adrenalectomy; bilateral hyperplasia → mineralocorticoid receptor antagonists (spironolactone, eplerenone). Important to distinguish from secondary hyperaldosteronism (elevated renin due to renal artery stenosis, heart failure, cirrhosis) which has high renin and high aldosterone. High-yield associations: hypertension + hypokalemia + metabolic alkalosis + low renin = primary hyperaldosteronism; think of Conn syndrome in resistant hypertension especially with unprovoked hypokalemia.