# Fibromuscular Dysplasia as a Cause of Secondary Hypertension: A Case Report

## TL;DR

A 39-year-old man with uncontrolled hypertension and stroke symptoms was found to have fibromuscular dysplasia, a rare cause of secondary hypertension.

## Contribution

This case highlights FMD as a potential cause of secondary hypertension and stroke in young adults.

## Key findings

- The patient's stroke and hypertension were linked to fibromuscular dysplasia in renal and carotid arteries.
- Imaging revealed a 'string-of-beads' appearance in renal arteries, characteristic of FMD.
- Medical management improved blood pressure and allowed partial neurological recovery.

## Abstract

Fibromuscular dysplasia (FMD) is characterized by the proliferation of connective tissue and smooth muscle fibers within the arterial wall, without inflammatory or atherosclerotic components, leading to stenosis, occlusion, or aneurysm formation and consequent impairment of perfusion in the affected organ. The renal, internal carotid, and vertebral arteries are most frequently involved. Secondary arterial hypertension and stroke are common clinical manifestations of FMD, as illustrated in the present case. A 39-year-old leucodermic male with a history of arterial hypertension, treated with amlodipine 10 mg and valsartan 160 mg, with poor compliance, presented to the emergency department with a one-week history of left-sided weakness and inability to walk. On examination, he was hypertensive (189/98 mmHg), with normal cardiac and pulmonary auscultation, left-sided hemiparesis predominantly affecting the leg, and a hemiparetic gait. Initial and 24-hour follow-up brain CT scans showed no evidence of acute ischemic or hemorrhagic lesions. ECG revealed sinus rhythm and voltage criteria for left ventricular hypertrophy. Echocardiography demonstrated left ventricular hypertrophy, left atrial dilation, and mild mitral regurgitation. Transcranial Doppler showed no right-to-left shunt. Brain MRI revealed an ischemic lesion in the right side of the pons, and magnetic resonance angiography demonstrated the absence of flow in the V4 segment of the left vertebral artery and reduced caliber of the left internal carotid artery. Laboratory tests showed worsening renal function after initiation of angiotensin-converting enzyme inhibitor therapy. Thrombophilia screening was negative. Due to suspected renal artery stenosis, CT angiography was performed, revealing saccular dilatations in both renal arteries with a “string-of-beads” appearance, suggestive of FMD. The patient was managed medically with blood pressure control. He began motor rehabilitation with partial recovery of neurological deficits and was discharged for follow-up in the outpatient clinic. In this patient, FMD was the underlying cause of the ischemic stroke that prompted hospitalization. The coexistence of difficult-to-control hypertension and target-organ damage in a young adult raised suspicion of secondary hypertension, and subsequent etiologic investigation led to the diagnosis of FMD.