A 56-year-old woman was referred with a history of poorly controlled hypertension of 5 years associated with hypokalemia, with potassium levels ranging from 2.1 to 3.0 mEq/L (the conversion from milliequivalents per liter to millimoles per liter is 1:1). Despite treatment with 2 mg of prazosin hydrochloride twice daily and 100 mg of atenolol every morning, her blood pressure remained elevated at 150/100 mm Hg. Her potassium levels could only be maintained at 3.5 mEq/L with 1200 mg of potassium replacement per day. Biochemical testing demonstrated a suppressed plasma renin activity of 150 pg/mL per hour (reference range, 660-3080 pg/mL per hour; to convert picograms per milliliter to picomoles per liter, multiply by 0.0237) and an elevated plasma aldosterone concentration of 33.2 ng/dL (reference range, 0.6-21.9 ng/dL; to convert nanograms per deciliter to picomoles per liter, multiply by 27.74). The elevated aldosterone to renin ratio of 221 supported a diagnosis of primary hyperaldosteronism (PH). A postural study after salt loading for 3 days was subsequently performed. This was inconclusive as the rise in the plasma aldosterone concentration was less than 30%. The biochemical results at 8 AMin the supine position were as follows: plasma aldosterone concentration, 30.0 ng/dL; plasma renin activity, 150 pg/mL per hour; and cortisol concentration, 11.5 μg/dL (to convert micrograms per deciliter to nanomoles per liter, multiply by 27.588). At 12 PMin the erect position, the results were as follows: plasma aldosterone concentration, 35.8 ng/dL; plasma renin activity, 70 pg/mL per hour; and cortisol concentration, 16.9 μg/dL. Computed tomography of the adrenal glands was performed (Figure) and the patient underwent adrenal venous sampling with corticotropin infusion, which demonstrated lateralization of aldosterone secretion to the left. The left-to-right cortisol-corrected aldosterone ratio was 13.5:1.