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A 59-year-old man is evaluated for recently discovered spontaneous hypokalemia and hypertension. The patient had normal blood pressure at a visit 1 year ago. He has no symptoms and takes no medications.
On physical examination, temperature is 36.9 °C (98.4 °F), blood pressure is 148/96 mm Hg, pulse rate is 58/min, respiration rate is 18/min, and BMI is 25. Examination findings are otherwise unremarkable.
The serum potassium level is 2.9 mEq/L (2.9 mmol/L) with increased urine potassium losses. After correction of the hypokalemia, the serum aldosterone level is 28.7 ng/dL (792 pmol/L) and the serum aldosterone to plasma renin activity ratio is 287. The serum aldosterone level is not suppressible with a high-sodium diet.
A CT scan of the adrenal glands shows minimal bilateral enlargement, with no identifiable masses or nodules.
Which of the following is the most appropriate initial treatment?
A) Bilateral adrenalectomy
B) Lisinopril
C) Spironolactone
D) Triamterene
MKSAP Answer and Critique
The correct answer is C) Spironolactone. This item is available to MKSAP 15 subscribers as item 97 in the Endocrinology and Metabolism section.
MKSAP 16 released Part A on July 31. More information is available online.
Spironolactone therapy should be initiated in this patient. He has biochemical findings suggestive of primary hyperaldosteronism. The initial clue to the diagnosis is the unprovoked hypokalemia and urine potassium renal losses. The results of laboratory studies show an elevated serum aldosterone level and suppressed plasma renin activity, which are suggestive of hyperaldosteronism. The diagnosis is usually confirmed by using a salt load to find out if aldosterone secretion is nonsuppressible and therefore autonomous. After primary hyperaldosteronism is biochemically confirmed, the cause should be defined. CT of the adrenal glands is an excellent way to localize an adrenal adenoma. This patient’s CT scan does not show an aldosterone-secreting adrenal adenoma but rather suggests bilateral adrenal hyperplasia. The treatment of choice in such instances is an aldosterone receptor–blocking agent, such as the nonselective agent spironolactone or the more selective agent eplerenone. Besides blocking aldosterone receptors, spironolactone usually lowers blood pressure and keeps it down. The combination of spironolactone with a thiazide diuretic may provide even better control and allow for smaller doses of spironolactone. If additional antihypertensive therapy is needed, calcium-channel blockers or angiotensin-converting enzyme inhibitors may be used.
Bilateral adrenalectomy is unnecessary and inappropriate in this patient with bilateral adrenal enlargement. Such treatment would make him dependent on permanent glucocorticoid and perhaps mineralocorticoid replacement therapy.
Beginning lisinopril therapy is unlikely to control the patient’s hypertension or address his primary hyperaldosteronism as well as an aldosterone blocker will.
Triamterene is a commonly used potassium-sparing diuretic that does not block the effects of aldosterone on the kidney. Using it will not be sufficient in this patient with hyperaldosteronism.
Key Point
- Primary hyperaldosteronism caused by bilateral adrenal hyperplasia is best treated medically with a nonselective (spironolactone) or more selective (eplerenone) aldosterone-blocking agent.
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