A patient with an aldosterone-producing adenoma has marked hypertension, hypokalemic alkalosis, and suppressed plasma renin, yet develops no peripheral edema over years. Which mechanism accounts for this resistance to salt retention?

• A Increased renal tubular reabsorption of potassium offsetting sodium retention
• B Downregulation of epithelial sodium channels in the collecting duct
• C Autonomous suppression of renin reducing angiotensin II below levels needed for aldosterone action
• D Atrial natriuretic peptide release and pressure natriuresis once volume expands ✓

Explanation

Mineralocorticoid escape limits volume expansion in primary aldosteronism: rising arterial pressure triggers pressure natriuresis, and atrial stretch releases ANP, which promotes sodium excretion. Escape operates when aldosterone is driven by non-volume mechanisms, whereas in secondary hyperaldosteronism (heart failure, cirrhosis, nephrosis) low arterial filling blunts these defenses and edema forms. Renin suppression is a marker of the disease, not the escape mechanism itself.

Reference: Guyton and Hall Textbook of Medical Physiology, 14th ed.

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