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Primary hyperaldosteronism — ABIM Board MCQ

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ModerateEndocrinology/MetabolismPrimary hyperaldosteronismABIM Board

A 49-year-old woman has a blood pressure of 168/96 mm Hg despite treatment with three antihypertensive agents. She is not taking a diuretic or mineralocorticoid receptor antagonist. Serum potassium is 3.1 mEq/L, and serum bicarbonate is 31 mEq/L. Plasma aldosterone concentration is 28 ng/dL, and plasma renin activity is 0.2 ng/mL/h. CT of the abdomen shows a 1.6-cm left adrenal adenoma. Which of the following diagnoses best explains these findings?

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Correct answer: E — Primary hyperaldosteronism

The correct answer is primary hyperaldosteronism. Autonomous aldosterone secretion causes sodium retention and hypertension while increasing renal potassium and hydrogen-ion excretion, producing hypokalemia and metabolic alkalosis. Volume expansion suppresses renin, so the combination of elevated aldosterone and suppressed renin is decisive. The adrenal adenoma suggests a possible aldosterone-producing adenoma, although CT alone does not establish functional laterality; adrenal venous sampling is generally used if surgery is contemplated. Renal artery stenosis causes secondary hyperaldosteronism with elevated renin. Liddle syndrome produces low renin and low aldosterone. Pheochromocytoma does not cause this mineralocorticoid biochemical pattern, and Cushing disease would require evidence of cortisol excess rather than elevated aldosterone.

Reference: Adler GK, et al. Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology & Metabolism. 2025;110(9):2453-2495. https://pubmed.ncbi.nlm.nih.gov/40658480/