Primary aldosteronism
USMLE Step 1Difficulty: mediumLast updated:
A 46-year-old woman is evaluated for hypertension that remains at 164/98 mm Hg despite treatment with three antihypertensive drugs. She reports episodic muscle weakness and nocturia. Serum studies show sodium 145 mEq/L, potassium 2.9 mEq/L, and a plasma aldosterone concentration of 31 ng/dL. CT of the abdomen shows a 1.6-cm nodule in the left adrenal gland; the renal arteries appear normal.
Which of the following combinations of findings is most likely in this patient?
Answer and explanation
Correct answer: B. Low plasma renin activity and metabolic alkalosis
This patient has autonomous aldosterone secretion from an adrenal nodule (primary aldosteronism). Aldosterone promotes sodium retention and potassium and hydrogen-ion excretion in the distal nephron. The resulting sodium and water retention expands blood volume, which suppresses renin release from the juxtaglomerular cells. The source states that patients with primary aldosteronism typically have plasma aldosterone > 15 ng/dL with low plasma renin activity (PRA) and an aldosterone-to-PRA ratio > 20. The same source notes that hypernatremia, hypervolemia, and a hypokalemic alkalosis may occur, causing episodic weakness, paresthesias, transient paralysis, and tetany, which matches this patient's weakness and potassium of 2.9 mEq/L. A high renin with high aldosterone would instead suggest secondary hyperaldosteronism (e.g., renal artery stenosis), which is unlikely with normal renal arteries and an adrenal nodule.
Each option explained
- A. High plasma renin activity and metabolic alkalosisIncorrect. High renin with hypokalemic alkalosis describes secondary hyperaldosteronism (e.g., renovascular hypertension); this patient has an adrenal source with normal renal arteries.
- B. Low plasma renin activity and metabolic alkalosisCorrect. Autonomous aldosterone secretion suppresses renin and causes hypokalemic metabolic alkalosis.
- C. Low plasma renin activity and metabolic acidosisIncorrect. Low renin with metabolic acidosis (and hyperkalemia) fits hyporeninemic hypoaldosteronism, the opposite hormonal state.
- D. Normal plasma renin activity and respiratory alkalosisIncorrect. Renin is suppressed in primary aldosteronism, and the acid-base disturbance is metabolic, not respiratory.
- E. High plasma renin activity and metabolic acidosisIncorrect. Renin is suppressed, not elevated, by the volume expansion of primary aldosteronism, and aldosterone excess causes alkalosis rather than acidosis.
Key point
Primary aldosteronism produces high aldosterone with suppressed renin and a hypokalemic metabolic alkalosis.
From the source
“Patients with primary aldosteronism typically have plasma aldosterone > 15 ng/dL ( > 0.42 nmol/L) and low levels of PRA, with a ratio of plasma aldosterone (in ng/dL) to plasma renin activity (in ng/mL/hour) > 20.”