This case highlights the diagnostic challenge of coexisting secondary causes of hypertension and the importance of reassessing the differential diagnosis when treatment fails to yield expected clinical improvement.
Supports reassessment for coexisting secondary hypertension causes; hypothesis-generating and should not change practice.
A 24-year-old woman with no prior comorbidities presented with severe, treatment-resistant hypertension characterized by episodic headaches and persistent systolic blood pressures above 140 mm Hg despite lifestyle modifications. Initial evaluation revealed hypokalemia and metabolic alkalosis with an aldosterone-to-renin ratio suggestive, but not diagnostic, of primary hyperaldosteronism. Secondary workup excluded pheochromocytoma, Cushing's syndrome, and thyroid disease. Imaging identified right renal artery fibromuscular dysplasia with angiographic narrowing of approximately 30%. Despite maximal medical therapy, her hypertension persisted, and repeat studies later demonstrated progression of stenosis to 70-75%, prompting angioplasty. The intervention improved arterial patency but failed to normalize her blood pressure or correct her tendency toward hypokalemia. Re-evaluation demonstrated a 1.7-cm left adrenal mass, and adrenal venous sampling confirmed unilateral aldosterone hypersecretion. The patient underwent laparoscopic adrenalectomy with pathology confirming an aldosterone-producing adenoma. Following surgery, she achieved normalization of potassium and sustained normotension without antihypertensive medications. This case highlights the diagnostic challenges when two secondary causes of hypertension coexist. Fibromuscular dysplasia initially diverted attention from primary hyperaldosteronism, delaying definitive diagnosis and curative treatment. Persistently suppressed renin and unexplained hypokalemia in the setting of uncontrolled hypertension, even after renal revascularization, should prompt clinicians to revisit the possibility of primary aldosteronism. This case underscores the importance of avoiding premature closure, maintaining vigilance for multiple etiologies, and reassessing the differential diagnosis when treatment of a plausible condition does not yield the expected clinical improvement.
No takes yet. Share an insight, caveat, or question.
Wurtz et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: