A 60-year-old patient has serum renin activity 0.4 ng/mL/hr (low) and serum aldosterone 32 ng/dL (high). She is hypertensive with hypokalemia. This biochemical pattern is most consistent with:

• A Primary hyperaldosteronism (Conn's syndrome) with autonomous aldosterone secretion suppressing renin ✓
• B Renovascular hypertension (renal artery stenosis) causing high renin, high aldosterone
• C Bartter syndrome with secondary aldosteronism and low-normal blood pressure
• D ACTH-dependent Cushing's syndrome causing mineralocorticoid excess

Explanation

The combination of low plasma renin activity (PRA) + high aldosterone + hypertension + hypokalemia is diagnostic of primary hyperaldosteronism (Conn's syndrome). Autonomous aldosterone secretion (from adrenal adenoma or bilateral hyperplasia) causes: (1) Na+ retention → volume expansion → hypertension; (2) K+ wasting → hypokalemia; (3) volume expansion suppresses renin via negative feedback (low PRA is a key feature). Renovascular hypertension has HIGH renin (renal ischemia activates RAAS). Bartter syndrome has high renin, high aldosterone but LOW blood pressure (because the tubular defect reduces NaCl reabsorption, preventing volume overload despite aldosterone). Cushing's syndrome causes hypertension via cortisol's mineralocorticoid effect, but renin is typically suppressed and aldosterone may be normal.

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

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