Fibromuscular dysplasia presenting as a renal infarction: a case report

<p>Abstract</p> <p>Introduction</p> <p>Fibromuscular dysplasia is a non-atherosclerotic, non-inflammatory disease that most commonly affects the renal and internal carotid arteries.</p> <p>Case presentation</p> <p>We present the case of a 44-year-old Caucasian man who was admitted with complaints of loin pain and hypertension. A computed tomography scan of the abdomen revealed a right renal infarction with a nodular aspect of the right renal artery. Subsequent renal angiography revealed a typical 'string of beads' pattern of the right renal artery with thrombus formation. Oral anticoagulation was started and the secondary hypertension was easily controlled with anti-hypertensive drugs. At follow-up, our patient refused percutaneous transluminal renal angioplasty as a definitive treatment.</p> <p>Conclusions</p> <p>Fibromuscular dysplasia is the most common cause of renovascular hypertension in patients under 50 years of age. Presentation with renal infarction is rare.</p> <p>In fibromuscular dysplasia, angioplasty has been proven to have, at least for some indications, an advantage over anti-hypertensive drugs. Therefore, hypertension secondary to fibromuscular dysplasia is the most common cause of curable hypertension.</p

A young man with a renal colic

We report the case of a 35-year-old man with no cardiovascular morbidity, presenting with acute flank pain, microscopic haematuria and normal blood pressure. Initially diagnosed as a ureteral colic, the patient was recovered 6 weeks later with severe hypertensive crisis. Further investigations revealed a massive renal infarction secondary to medial fibromuscular dysplasia (FMD). Several aspects of this presentation are intriguing. Renal infarcts are usually seen in older patients having cardiac problems and/or major atheromatous plaques. In addition, FMD is mainly observed in young females and rarely progresses to renal artery occlusion. Furthermore, in this case, FMD remained silent until the acute renal infarction occurred, despite a significant kidney size reduction at the time of diagnosis. Finally, the observation of a delayed hypertensive response to a major renovascular insult provides incentives to discuss possible pathophysiological mechanisms involved in renovascular hypertension