Not Just One Answer: A Case of Resistant Hypertension with Overlapping Etiologies

Introduction: Hypertension (HTN) is a leading modifiable risk factor for cardiovascular morbidity and mortality. Despite an increase in social awareness, many patients fail to achieve a target blood pressure (BP). In resistant hypertension, identifying a secondary cause can often help guide treatment and improve clinical outcomes. Here we present a case of resistant hypertension in a patient with coexisting renal artery stenosis in a solitary functioning kidney as well as hyperaldosteronism. Case Description: A 73-year-old white male with history of long-standing HTN, atrophic left kidney due to nephrolithiasis, OSA on CPAP, hypertrophic cardiomyopathy presented with uncontrolled HTN. He denied secondary symptoms. Despite adherence to a low sodium diet, CPAP and a six-drug regimen including amlodipine 10mg, metoprolol 150mg, lisinopril 40mg, terazosin 20mg, chlorthalidone 25mg, and spironolactone 25mg daily, BP remained elevated at 160-180/80-90 mm Hg. He denied NSAID use, smoking or any other illicit substance use. Work-up was significant an elevated aldosterone: 35.4ng/dl, suppressed direct renin: 2.1pg/ml with aldosterone to renin ratio(ARR): 16.9 consistent with a diagnosis of hyperaldosteronism. CT scan revealed bilateral adrenal hyperplasia. Renal artery US showed 60-99% right renal artery stenosis in the setting of a solitary functioning kidney. For his hyperaldosteronism, spironolactone was increased to 100mg daily and chlorthalidone was discontinued. BP improved but remained elevated at 160/80 mm Hg. Renin normalized with optimized spironolactone. The patient subsequently underwent renal artery stenting, following which BP improved to goal 120/80 mm Hg, allowing de-escalation of antihypertensives to spironolactone 25mg daily. He remained on metoprolol ER 50mg, diltiazem 240mg, furosemide 20mg daily for his hypertrophic cardiomyopathy. Discussion: Timely evaluation and management of hypertension are crucial to reducing the risk of cardiovascular events. In our case, a systematic work-up revealed a dual cause of resistant hypertension, including primary hyperaldosteronism with bilateral adrenal hyperplasia managed with optimal dose of spironolactone. A concurrent renal artery stenosis was managed with angioplasty that helped bring his BP to goal. With this case, we highlight the importance of identifying and understanding the pathophysiology of secondary causes of resistant hypertension.