Case Presentation: A 40-year-old woman with history of persistent severe hypertension despite multiple antihypertensive agents, chronic renal dysfunction due to single functional kidney , and calcific arterial disease (coral reef aorta) requiring previous aortobifemoral bypass presented to the hospital with oliguria, a blood pressure of 240/110 mmHg and hypertensive emergency as evidenced by acutely worsened renal function. Her creatinine was 4.7 mg/dL (baseline 1.7mg/dL). Home medications included high dose carvedilol, hydralazine, nifedipine and isosorbide mononitrate and she reported adherence. CT angiography was suggestive of severe renal artery stenosis (RAS) so she was taken to the OR emergently for renal artery stent placement. Immediately post procedure her urine output significantly increased and the same day her isosorbide was discontinued and hydralazine dose reduced due to improved blood pressure. At the time of discharge, her blood pressure was well controlled on carvedilol alone and creatinine had improved to better than her baseline.

Discussion: Our patient suffered from uncontrolled hypertension despite being on multiple medications, which should make a hospitalist suspicious for secondary causes of hypertension. RAS should be suspected when hypertension is discovered before age 30 or when it is severe after age 50 AND is accelerated, resistant to treatment, or causing end organ damage. Other clues include an unexplained atrophic kidney or renal dysfunction, both of which our patient had. In general, RAS affects 1 to 5% of the general population with hypertension and is a well-established cause of secondary hypertension. Usually the risk of RAS increases with age and the presence of other cardiovascular risk factors. The longer stenosis persists the more likely the patient is to experience renal atrophy, and one study suggests 60% of untreated stenoses lead to 21% of atrophy of affected kidneys. There are no clear guidelines on how to treat RAS. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers are considered first line antihypertensive therapy for RAS; however in a patient with only one solitary kidney as our patient, these medications may lead to acute renal failure and are generally avoided. Renal revascularization is more controversial because not all patients achieve clinical benefit that outweighs the risk of the procedure, but it should be considered when renal function is at risk.

Conclusions: We present a patient with RAS presenting with renal failure and hypertensive emergency. Even though no clear guidelines exist for treatment for RAS she underwent emergent revascularization and her favorable response suggests that in extreme situations, extreme measures must be taken. This case illustrates that more research is needed on the appropriate treatment of RAS in specific circumstances, be it medical, surgical or a combination of both.