Match each laboratory and hormonal profile to the most likely secondary cause of hypertension.
- Elevated plasma aldosterone concentration, decreased plasma renin activity, and spontaneous hypokalemia.Primary hyperaldosteronism (e.g., Conn syndrome)
- Elevated plasma aldosterone concentration, elevated plasma renin activity, and spontaneous hypokalemia.Secondary hyperaldosteronism (e.g., renal artery stenosis)
- Decreased plasma aldosterone concentration, decreased plasma renin activity, and spontaneous hypokalemia.Syndrome of apparent mineralocorticoid excess (e.g., licorice toxicity)
- Normal plasma aldosterone, normal plasma renin activity, normal potassium, and elevated plasma fractionated metanephrines.Pheochromocytoma
Answer
The secondary causes of hypertension map to their specific hormonal patterns: Primary hyperaldosteronism (elevated aldosterone, low renin), Secondary hyperaldosteronism (elevated aldosterone, elevated renin), Apparent mineralocorticoid excess (low aldosterone, low renin), and Pheochromocytoma (elevated metanephrines, normal RAAS).
Each laboratory pattern distinctively maps to the underlying pathophysiology. Primary hyperaldosteronism involves autonomous aldosterone production that suppresses renin. Secondary hyperaldosteronism begins with renin overproduction that subsequently drives aldosterone. Apparent mineralocorticoid excess mimics aldosterone, appropriately suppressing both native renin and aldosterone. Pheochromocytoma acts via catecholamines, leaving the renin-aldosterone axis intact while producing elevated metanephrines.
Step-by-Step Solution
Key Concept
Interpretation of the renin-angiotensin-aldosterone system and related hormonal panels in secondary hypertension.