Successful Angioplasty and Stenting of an Unusual Case of Bilateral Renal Artery Stenosis

Abstract

We report a case of acute renal failure secondary to bilateral renal artery stenosis (RAS) presenting with anuria and well-controlled blood pressure. Renal function improved following percutaneous transluminal angioplasty and stenting (PTA/S). Anuria and well-controlled blood pressure can be an unusual presentation of bilateral RAS, and early detection followed by angioplasty and stenting in this group of patients may lead to an improvement in blood pressure control and preservation of renal functions.

Introduction

Atherosclerotic renal artery stenosis (RAS) is most often caused by plaque formation in the abdominal aortic wall, with progression into the proximal renal artery lumen. Prevalence of RAS increases with age and is associated with diabetes, hyperlipidemia, and hypertension.1 Bilateral RAS can present with renal dysfunction and typically uncontrolled or poorly controlled blood pressure, despite the use of multiple antihypertensive agents. We describe an unusual case of severe bilateral RAS presenting with acute renal failure, anuria, and well-controlled blood pressure that was successfully treated with percutaneous transluminal angioplasty and stenting (PTA/S).

Case Report

A 72-year-old caucasian male with multiple comorbidities, including hypertension, diabetes mellitus type II, coronary artery disease, chronic atrial fibrillation, and hyperlipidemia presented to the emergency department with a 3-day history of anorexia associated with anuria. Blood pressure at presentation was 120/72 mmHg. On medical record review, his average systolic/diastolic blood pressure in the last 2–3 years was 124 ± 10/72 ± 12 mmHg with a baseline serum creatinine of 1.1–1.2 mg/dL. The patient was compliant with his medications (atenolol, lisinopril, and hydrochlorothiazide) and denied using nonsteroidal, anti-inflammatory drugs. On physical examination, jugular venous distension, fine-end inspiratory crackles at the lung bases and bilateral, pitting, pedal edema were evident. An abdominal bruit was not appreciated. Laboratory evaluation showed serum potassium of 7 mEq/L, serum creatinine of 9 mg/dL, and blood urea nitrogen (BUN) of 60 mg/dL. By comparison, a week prior to admission, the serum creatinine and BUN were 1.2 mg/dL and 22 mg/dL, respectively. International normalized ratio (INR) was 4.8, secondary to oral anticoagulant therapy for chronic atrial fibrillation. A duplex ultrasound of the kidneys revealed poor direct visualization of the renal arteries. An indirect study of the upper, mid, and lower pole segmental arteries bilaterally was consistent with proximal bilateral RAS and the absence of parenchymal disease. The kidney size was normal, with the dimensions being 10.63 cm on the right and 10.01 cm on the left. Intravenous furosemide was instituted, which facilitated minimal urine output, while creatinine and BUN continued to rise. Evaluation by digital subtraction angiography (DSA) using a 1:4 mixture of iodixanol (20 cc) (VISIPAQUE,TM GE Healthcare, Princeton, New Jersey) and gadolinium (80 cc) confirmed severe bilateral RAS. The right renal artery had an 80% ostial tubular stenotic lesion, with a mean resting gradient of 30 mm Hg measured with a 4 Fr catheter. A 7-Fr, 50-cm RDCI VERIPATH (Abbott Vascular, Abbott Park, Illinois) guiding catheter was placed at the ostium of the vessel. Stenting was performed with a 6.5 x 18 mm cobalt-chromium, balloon-expandable, bare-metal stent at 12 atmospheres for 10 seconds (Herculink ELITE RX plus™; Abbott Vascular) with the use of an EPD, 6.5 mm Rx ACCUNET 2TM (Abbott Vascular). This resulted in a 0% residual stenosis and 0 mm Hg resting gradient. The left renal artery had a 99% tubular stenotic lesion at the proximal end, with a mean-resting gradient of 60 mm Hg. A 7-Fr, 50-cm RDCI VERIPATH guiding catheter was placed at the ostium of the vessel. A 6.0 x 18 mm cobalt-chromium (Herculink ELITE RX plusTM) balloon-expandable, bare-metal stent was inserted at 12 atmospheres for 10 seconds with use of an EPD, 6.5 mm RX ACCUNET 2 Embolic Protection System, with a subsequent 0% residual stenosis and 0 mm Hg resting gradient.

The patient received pre-intervention intravenous hydration with sodium bicarbonate drip. Serum creatinine improved over the following two weeks from 9 mg/dL pre-intervention to 1.1 mg/dL (baseline) post-intervention and BUN similarly decreased from 60 mg/dL to 24 mg/dL. The strongest predictor of the recovery of renal function was the rate of decline of the serum creatinine and the BUN. Angiotensin-converting enzyme inhibitors (ACEi) were held from the time of presentation until normalization of the renal functions. The patient was subsequently discharged on atenolol, hydrochlorothiazide, and lisinopril, however, the dosage of atenolol was reduced from 25 to 12.5 mg over the next month, and hydrochlorothiazide and lisinopril were discontinued 1 month following renal stent placement, due to excellent control of the blood pressure with a single agent (i.e., atenolol). Clopidogrel was continued for 2 months post-intervention. Blood pressure continued to range from 100–110/50–60 mm Hg. Serum creatinine remained normal over the ensuing 10 months.

Discussion

Anuria and well-controlled blood pressure may be an unusual manifestation of severe bilateral RAS. Prerenal azotemia is considered a functional response to renal hypoperfusion in which renal structure and microstructure are preserved. Autoregulation in the kidneys maintains a normal glomerular filtration rate (GFR) and blood flow, even with a mean arterial pressure as low as 80 mm Hg. This derives mainly from the drop in resistance of afferent arterioles and to a lesser extent, increased resistance in the efferent arterioles. As the perfusion pressure drops further (to