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Kidney Week

Abstract: PO0328

Renal Failure due to Bilateral Renal Artery Stenosis

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Janosevic, John, Hunter College, New York, New York, United States
  • Martinez Lopez, Maria Fernanda, Universidad Iberoamericana, Santo Domingo, Dominican Republic
  • Janosevic, Danielle, Indiana University School of Medicine, Indianapolis, Indiana, United States

We present a patient with renal failure and accelerated hypertension while on a chronic, stable dose of an angiotensin-converting enzyme inhibitor (ACEI) due to progression of renal artery stenosis (RAS).

Case Description

A 73 year-old Caucasian male with DM2, HLD, CKD2 was referred for evaluation of resistant HTN. Initial visit, blood pressure (BP) was controlled on stable doses of metoprolol XR 50 mg qd, amlodipine 10 mg qd, hydrochlorothiazide 25 mg qd and lisinopril 40 mg qd. Ultrasound revealed bilateral 11 cm kidneys, left proximal RAS with peak systolic velocities (PSV) of 2.6 m/s, globally elevated resistive indices (RI) >0.83-0.86. Given controlled HTN, stable renal function with baseline Scr range of 1.1-1.2, he was conservatively managed with above medications and statin. On 4 month follow up, BP 160-200/60s, despite stable medication doses and compliance, unexplained elevated Scr 2.1 mg/dL. Given suspicion of RAS progression, renin and aldosterone level were drawn measuring 3000 pg/ml (6 mo prior 1800) and 16 ng/dl (prior 12), respectively. Patient underwent renal artery duplex with noted bilateral RAS: >60% diameter reductions and RI averaging 0.85. ACEI was promptly discontinued and within 48 hours, the patient’s Scr improved to 1.5, and he underwent CT-Angiogram (CTA) abdomen to determine if intervention needed. CTA noted bilateral moderate ostial RAS (left 50%, right 30%) due to progression of atherosclerotic calcifications. At follow up, Scr normalized to 1.2, BP controlled on amlodipine 10 mg qd and carvedilol 3.125 mg BID. Given the resolution of uncontrolled resistant HTN, and return to baseline Scr, renal artery stenting was not pursued and the decision remained continued monitoring.


ACEI are indicated as effective anti-HTN therapy in unilateral RAS. However, when accelerated hypertension and/or renal failure occurs while on an ACEI in an elevated risk individual with RAS, a high index of suspicion for RAS progression must be entertained and the ACEI promptly discontinued. Individuals at risk for progression of atherosclerotic lesions are elderly individuals, especially those with HLD and DM. Elevated renin levels and Scr, which were rapidly obtainable during our clinic visit, were suggestive of pronounced renal ischemia and prompted quick action of ACEI discontinuation, definitive imaging and overall clinical improvement.