A 30-year-old previously healthy man is evaluated for fatigue, muscle weakness, and occasional headaches over the past several months. Blood pressure is 180/110 mm Hg, and pulse is 80/min. Laboratory evaluation reveals low serum potassium and markedly depressed plasma renin activity. CT scan of the abdomen demonstrates a right-sided adrenal mass. Treatment options are discussed, and pharmacologic therapy is begun. On a follow-up visit after several weeks of treatment, the patient reports improvement of his symptoms. Blood pressure is 130/70 mm Hg, and pulse is 75/min. Which of the following medications was most likely prescribed to this patient?
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This patient's new-onset hypertension, symptomatic hypokalemia (eg, fatigue, muscle weakness), and low plasma renin activity are indicative of primary hyperaldosteronism. Primary hyperaldosteronism involves unregulated aldosterone secretion, typically due to either an adrenal adenoma—as suggested by this patient's CT finding of a unilateral adrenal mass—or bilateral adrenal hyperplasia.
Aldosterone, which is a mineralocorticoid normally regulated by angiotensin II and potassium (K+) levels, stimulates reabsorption of sodium (Na+) and secretion of K+ and hydrogen (H+) in the renal collecting ducts. Excess aldosterone therefore causes intravascular volume retention and hypertension (which can cause headache if severe), in addition to predisposing to hypokalemia and metabolic alkalosis. Depressed plasma renin activity also occurs due to feedback suppression of the renin-angiotensin-aldosterone system.
An adrenal adenoma is typically treated with adrenalectomy; however, patients who are not surgical candidates or those who decline surgery can be treated with a mineralocorticoid receptor antagonist (MRA). MRAs block the effects of excess aldosterone, thereby reducing blood pressure and treating hypokalemia and metabolic alkalosis. Spironolactone is most commonly used; eplerenone is less likely to cause adverse endocrine effects (eg, gynecomastia, decreased libido).
(Choices A, B, C, D, E, F, and H) Other antihypertensive medications are unlikely to normalize blood pressure in patients with primary hyperaldosteronism because these medications do not address the excess levels of aldosterone. Inhibitors of the renin-angiotensin-aldosterone system other than MRAs (eg, ACE inhibitors, beta blockers) have little effect on aldosterone levels in these patients because aldosterone release is autonomous and independent of angiotensin II stimulation.
Educational objective:
Primary hyperaldosteronism involves excess aldosterone secretion, which causes hypertension and predisposes to hypokalemia and metabolic alkalosis; low plasma renin activity helps distinguish it from other causes of excess aldosterone (eg, renovascular disease). First-line medical therapy for primary hyperaldosteronism includes mineralocorticoid receptor antagonist (eg, spironolactone, eplerenone).