Percutaneous Renal Intervention Utilizing Distal Embolic Protection

Background. A 74-year-old female was referred for further evaluation of accelerated hypertension. She had a long history of well controlled hypertension, but more recently had blood pressure readings as high as 200/100 mmHg. There was no associated anginal chest pain, symptoms of congestive heart failure, or neurologic symptoms. Her past medical history was remarkable for coronary artery disease with coronary artery bypass grafting in 1992, a transient ischemic attack in 1998, and hyperlipidemia. There was no prior history of tobacco use, diabetes, or renal insufficiency. Her medications included atenolol 50 mg q day, accupril 30 mg q day, hydrochlorothiazide 25 mg per day, and aspirin 81 mg per day. Physical exam demonstrated a resting blood pressure of 180/86 mmHg. Otherwise, the examination was unremarkable. A multirow detector CT scan revealed solitary bilateral renal arteries with mild calcified plaquing in the abdominal aorta. There was a focal 70% stenosis at the ostium of the left renal artery with mild calcified plaquing at the ostium of the right renal artery. Both kidneys appeared to be of relative equal size. Angiogram and intervention. Routine abdominal aortogram was performed using a pigtail catheter via a 6 French (Fr) right common femoral access. Bilateral selective renal angiography was completed with a JR4 diagnostic catheter. The infra-renal abdominal aorta had mild to moderate calcified plaquing with mild ectasia in the distal segment. Both renal arteries were solitary. The left renal artery had an ostial 80% narrowing with diffuse 25–30% disease distally (Figure 1). It was relatively tortuous, but had a long segment before any major branches. The right renal artery had an ostial 40–50% narrowing, also with diffuse 25–30% disease distally. The patient gave her informed consent to participate in the RESIST (Embolic Protection and Platelet Inhibition During Renal Artery Stenting) study. An 8 Fr RDC guide was utilized. She was given boluses of heparin until the activated clotting time (ACT) was greater than 300 seconds. She was then given the study drug which was either placebo or the glycoprotein (GP) IIb/IIIa inhibitor abciximab (ReoPro, Eli Lilly, Indianapolis, Indiana). She was randomized to have the intervention performed utilizing a distal embolic protection device. A 7 mm AngioGuard (Cordis Endovascular, Warren, New Jersey) was deployed in the distal left renal artery. Due to the severe angulation of proximal segment of the artery, there was some difficulty advancing the filter. However, this was accomplished successfully without causing a dissection (Figure 2). The lesion was predilated with a 5 x 20 mm balloon, and then stented with a 6 x 12 mm balloon expandable stent. The stent was deployed at 6 atmospheres (atm), and the proximal edge was post-dilated up to 10 atm. The filter was retrieved without difficulty. There was no visible debris seen in the filter. There was 0% residual stenosis with excellent antegrade flow and no dissection (Figure 3). Approximately 125 mL of iso-osmolar, non-ionic contrast was administered. A closure device was used and there were no complications of the procedure. The preprocedure creatinine was 1.3 mg/dL with a calculated creatinine clearance (CrCl) of 30 mL/minute, while the 24-hour post-procedure creatinine was 1.0 mg/dL with a calculated CrCl of 39 mL/minute. Follow up. At her 30-day follow-up visit she was having symptomatic hypotension with blood pressures as low as 90/46 mmHg. Accupril had been discontinued within the first week post procedure. The atenolol dose was subsequently decreased to 25 mg per day. At her 12-month visit she was maintaining a home blood pressure of approximately 100/60 mmHg on accupril 5mg per day, and atenolol 12.5 mg per day. Discussion. Renal artery stenosis is typically due to atherosclerotic disease and is a common cause of secondary hypertension and progressive renal insufficiency. Renal artery stenting (RAS) has become the preferred method of revascularization, however, acute deterioration in renal function occurs approximately 20% of the time following endovascular intervention. The renal insult can be severe enough to result in temporary or permanent dialysis. It has been hypothesized that acute renal insufficiency following renal artery stenting may be due to athero-embolization, platelet thrombo-embolization, or contrast nephrotoxicity. The use of distal embolic protection devices (EPDs) significantly decreases major adverse cardiac events during percutaneous coronary intervention. Several small studies have also suggested that using EPDs during RAS may be beneficial.1–3 RESIST Study. The Embolic Protection and Platelet Inhibition during Renal Artery Stenting (RESIST) study studied the relationship between embolic protection and the GP IIb/IIIa inhibitor abciximab (Eli Lilly, Indianapolis, Indiana) used during renal artery stenting.4 RESIST was a phase 2 safety and efficacy study that randomized 100 patients in a 2 x 2 factorial design between embolic protection with the AngioGuard (Cordis Endovascular, Warren, Nw Jersey) versus no EPD, and platelet inhibition with abciximab versus placebo. There were four groups: control, AngioGuard only, abciximab only, and AngioGuard and abciximab. The primary endpoint was the protection of renal function and preventing renal injury 1 month after RAS. The inclusion criteria were a history of hypertension, renal insufficiency, heart failure, or angina with poorly controlled hypertension with at least one renal artery stenosis > 50% and From the Midwest Cardiovascular Research Foundation, Davenport, Iowa. The author reports no conflicts of interest regarding the content herein. Manuscript submitted April 1, 2009, final version accepted April 15, 2009. Address for correspondence: Eric J. Dippel, MD, FACC, Midwest Cardiovascular Research Foundation, Cardiovascular Medicine, PC, 1236 E Rusholme Street, Davenport, IA 52803. E-mail: dippel@cvmedpc.com

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