The Silent Long-Term Damage of Resistant Hypertension: A Clinical Case Report

Background/Aim: Resistant hypertension (RH) is a complex clinical condition associated with substantial cardiovascular and renal morbidity. Persistent blood pressure (BP) elevation despite optimal multidrug therapy should prompt a careful search for secondary causes and hypertension-mediated target organ damage. Chronic kidney disease (CKD) and sustained activation of the renin–angiotensin–aldosterone system (RAAS) are frequently involved, often resulting in a prolonged subclinical course. This case report aims to highlight the clinical importance of a structured diagnostic approach to resistant hypertension in the context of a hypertensive emergency.

Case: A 56-year-old man without previous medical follow-up presented with severe hypertension accompanied by headache and epigastric discomfort. BP measurements revealed marked inter-arm differences and values consistent with a hypertensive emergency. Laboratory evaluation showed impaired renal function, hypokalemia, and significant proteinuria. Imaging and echocardiographic assessment demonstrated chronic kidney disease, left ventricular hypertrophy, pulmonary congestion, and ascending aortic dilatation. Further hormonal evaluation revealed elevated renin and aldosterone levels with a low aldosterone to renin ratio, supporting secondary hyperaldosteronism related to CKD and exacerbated by frequent nonsteroidal anti-inflammatory drug use. BP was controlled with intravenous antihypertensive therapy followed by intensive oral multidrug treatment, including diuretics, renin–angiotensin system blockade, and an aldosterone antagonist.

Conclusion: This case demonstrates that long-standing, undiagnosed hypertension may present as a hypertensive emergency accompanied by advanced target organ damage. Hypervolemia and the RAAS play a critical role in the development of RH, particularly when combined with CKD and nonsteroidal anti-inflammatory drug use. Low aldosterone to renin ratio levels, accompanied by elevated renin and aldosterone levels, serve as a valuable marker for ruling out primary adrenal pathology and indicate secondary hyperaldosteronism. Although the difference in BP between the arms initially suggests structural vascular abnormalities, the underlying etiology is RAAS activation triggered by CKD and hypervolemia. This case highlights the importance of regular BP measurements and a systematic approach, including assessment of the RAAS profile, fluid status, and medication history, for accurate diagnosis in RH.