Question of the Day
Monday, November 9, 2026
A 48-year-old woman comes to the physician because of headaches and muscle weakness for 4 months. She takes no medications. Her blood pressure is 172/104 mm Hg despite restriction of dietary sodium; other vital signs are within normal limits. Physical examination shows no edema. Serum studies show:
Na+ 146 mEq/L
K+ 2.9 mEq/L
Cl- 103 mEq/L
HCO3- 31 mEq/L
Arterial pH is 7.49. Plasma renin activity is markedly decreased and the plasma aldosterone concentration is markedly increased. CT of the abdomen shows a 1.5-cm unilateral adrenal mass.
Which of the following best explains this patient's hypokalemia and hypertension?
Answer: E. Stimulation of collecting duct sodium reabsorption and potassium secretion
The correct answer is E (Stimulation of collecting duct sodium reabsorption and potassium secretion). Hypertension with hypokalemia, metabolic alkalosis, high-normal sodium, markedly increased aldosterone with suppressed renin, and a unilateral adrenal mass indicate primary hyperaldosteronism from an aldosterone-producing adenoma (Conn syndrome). Aldosterone increases ENaC and Na+/K+-ATPase activity in principal cells of the cortical collecting duct; sodium reabsorption expands volume and raises blood pressure, and the lumen-negative potential drives potassium secretion through ROMK and proton secretion by intercalated cells. Edema is absent because of aldosterone escape.
Why not A (Decreased cortisol negative feedback on the pituitary): This describes primary adrenal insufficiency with high ACTH, which causes hypotension and hyperkalemia.
Why not B (Excess catecholamine release from chromaffin cells): Pheochromocytoma causes paroxysmal hypertension, headache, and sweating without high aldosterone and suppressed renin.
Why not C (Increased vascular sensitivity to angiotensin II from high renin): Renin is suppressed by volume expansion, which is what distinguishes primary from secondary hyperaldosteronism.
Why not D (Cortisol activation of renal mineralocorticoid receptors from 11β-HSD2 deficiency): Apparent mineralocorticoid excess (or licorice ingestion) causes the same electrolyte pattern, but aldosterone is suppressed, not elevated.
Clinical Pearl: Hypertension with hypokalemia and a high aldosterone-to-renin ratio is primary aldosteronism until proven otherwise.
Just show me the answer
Answer: E. Stimulation of collecting duct sodium reabsorption and potassium secretion
The correct answer is E (Stimulation of collecting duct sodium reabsorption and potassium secretion). Hypertension with hypokalemia, metabolic alkalosis, high-normal sodium, markedly increased aldosterone with suppressed renin, and a unilateral adrenal mass indicate primary hyperaldosteronism from an aldosterone-producing adenoma (Conn syndrome). Aldosterone increases ENaC and Na+/K+-ATPase activity in principal cells of the cortical collecting duct; sodium reabsorption expands volume and raises blood pressure, and the lumen-negative potential drives potassium secretion through ROMK and proton secretion by intercalated cells. Edema is absent because of aldosterone escape.
Why not A (Decreased cortisol negative feedback on the pituitary): This describes primary adrenal insufficiency with high ACTH, which causes hypotension and hyperkalemia.
Why not B (Excess catecholamine release from chromaffin cells): Pheochromocytoma causes paroxysmal hypertension, headache, and sweating without high aldosterone and suppressed renin.
Why not C (Increased vascular sensitivity to angiotensin II from high renin): Renin is suppressed by volume expansion, which is what distinguishes primary from secondary hyperaldosteronism.
Why not D (Cortisol activation of renal mineralocorticoid receptors from 11β-HSD2 deficiency): Apparent mineralocorticoid excess (or licorice ingestion) causes the same electrolyte pattern, but aldosterone is suppressed, not elevated.
Clinical Pearl: Hypertension with hypokalemia and a high aldosterone-to-renin ratio is primary aldosteronism until proven otherwise.
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