Primary hyperaldosteronism EXCEPT?

• A. High serum sodium
• B. High serum potassium
• C. Low plasma renin that fails to increase with volume depletion
• D. High aldosterone that fails to decrease with saline or angiotensin inhibition

Answer: (B)

The pattern being tested is how autonomous aldosterone excess affects kidney handling of electrolytes and the renin–angiotensin system. In primary hyperaldosteronism, excess aldosterone causes more sodium reabsorption and more potassium (and hydrogen) secretion in the distal tubule. That leads to mild hypernatremia and a tendency toward hypokalemia, along with metabolic alkalosis and hypertension. Because aldosterone is produced independently, plasma renin activity is suppressed and typically does not rise with volume depletion. Importantly, aldosterone remains high even when saline is given or angiotensin is inhibited, reflecting its autonomous production. Therefore, a statement claiming high serum potassium does not fit the typical profile; potassium is usually low, not high. The other statements align with the expected findings: elevated sodium, low renin that does not increase with volume depletion, and aldosterone that does not decrease with saline or angiotensin blockade.