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Case Report and Brief Review

Endovascular Treatment of a Renal Artery Aneurysm with Distal Stenosis: A Case Report and Review

February 2011
2152-4343

Abstract

Renal artery aneurysms (RAAs) are being diagnosed with increasing frequency. They can be incidental or symptomatic. Rupture is the most feared complication. RAAs can be managed conservatively or treated with either surgery or an endovascular approach. We present the case of a 48-year-old female who had a large RAA with a distal stenosis that was treated with a stent-graft. Two-year follow-up is available on this patient. A review of the literature is also presented.

VASCULAR DISEASE MANAGEMENT 2011;8(2):E45–E49

Key words: aneurysm repair; renal artery intervention; stent graft

Introduction

Visceral artery aneurysms (VAAs) are being diagnosed with increasing frequency as result of the expanding and widespread use of noninvasive imaging technologies (computed tomography [CT], magnetic resonance imaging [MRI] and ultrasonography). Renal artery aneurysms (RAAs) account for 15–25% of all VAAs and are the second or third most common VAAs.1 When diagnosed, treatment modalities include medical management, endovascular treatment or surgery. We present a case of an incidental, large RAA with a distal stenosis successfully treated with a stent-graft. Two-year follow-up information is provided.

Case Report

A 48-year-old female consulted her general physician for chronic hip and back pain. She had hypertension and had been under treatment with enalapril, with poor blood pressure control. She had a hypothyroid condition and was under hormonal replacement therapy. The patient was also a smoker. Spine and hip radiographs were ordered. A radiolucent mass was noted on her left flank. A CT scan was performed and showed a 2 cm diameter, calcified aneurysm located in the main left renal artery. Selective renal angiography was performed via retrograde femoral access with a 5 Fr JR catheter, and confirmed the presence of a 2.1 cm wide-necked saccular aneurysm located in the mid portion of the left renal artery. A tight stenosis distal to the aneurysm was noted, as well as circumferential calcification of the aneurysmal sac and a small superior branch emerging from the aneurysm (Figure 1). Two small intrarenal aneurysms were also seen. Her serum creatinine was normal. An 8 Fr introducer was placed in the right femoral artery. At the beginning of the procedure, heparin 5,000 IU were administered. An AquaLiner 0.035 inch hydrophilic wire (Nipro Corp., Osaka, Japan) was used to cross through the aneurysm and the stenosis. A 4 Fr JR catheter was advanced over the wire. Next, a Wholey 0.035 inch wire (Covidien, Mansfield, Massachusetts) was advanced through the 4 Fr catheter. A peripheral balloon was unable to cross the distal stenosis, so a Hi-Torque Floppy 0.014 inch Extra-Support wire (Abbott Vascular, Santa Clara, California) was advanced. Both wires were used to perform the buddy-wire technique, and a 3.5–40 mm coronary balloon was able to reach the stenosis and predilate it (Figure 2). The Wholey wire was then exchanged for an Amplatz Super-Stiff EX wire (Boston Scientific Corp., Natick, Massachusetts). Placement of 6–38 mm Advanta V12 stent-graft (Atrium Medical, Hudson, New Hampshire) was attempted, but was unsuccessful due to support difficulties. The guide catheter was replaced by a 7 Fr Destination 90 cm sheath (Terumo Interventional Systems, Somerset, New Jersey), which was advanced to the mid portion of the renal artery. After several attempts, the stent-graft was placed in an adequate position (Figure 3). The Advanta V12 stent-graft was then deployed at 12 atm. Underexpansion of the distal segment of the device was noted. A 7.0–20 mm Powerflex P3 peripheral balloon (Cordis Corp., Miami Lakes, California) was advanced to postdilate the stent. Immediate aneurysm exclusion was achieved without residual stenosis (Figure 4). Two procedure-related complications occurred. First, the occlusion of the small superior branch emerging from aneurysm was anticipated and inherent to the treatment modality. The second complication noted was a perforation of a small inferior branch produced by the Amplatz wire. The heparin effect was reversed with protamine, and serial angiograms showed a complete cessation of extravasation. Both complications were clinically and functionally silent, with no increase in serum creatinine. The patient was discharged 48 hours post angioplasty. On follow-up, the patient remained asymptomatic. Her blood pressure was controlled with amlodipine 5 mg daily and her renal functional test remained normal. Two years later, contrast CT angiography was performed and showed complete aneurysm exclusion without significant in-stent restenosis (Figure 5).

Discussion

In 1770, Rouppe found a large false renal aneurysm with rupture in an autopsy of a patient who died with right flank pain. This was the first published report of a renal artery aneurysm (RAA).2 Since that time, information about this rare entity has been provided in several case reports and series.3–6 Nowadays, the routine use of CT, MRI and ultrasonography has led to the increased diagnosis of RAAs. These are defined as a dilated segment of renal artery exceeding twice the normal renal artery diameter. Its true incidence in the general population is not clear. On autopsy studies, the reported incidence of RAAs is 0.01%.7 In angiographic series, the incidence varied between 0.3 and 0.7%.5,8,9 This difference between autopsy and angiographic series may be related to underdiagnosis of small intrarenal aneurysms on routine autopsies.5 They represent the second or third most common VAAs and account for 15–25% of them.1 RAAs are usually detected in 40- to 60-year-old patients, with equal gender distribution.9 The most common location of RAAs is the main renal artery. They can be classified as:

• True aneurysms: all layers of the artery are included in the aneurysm wall. They can be saccular or fusiform, and are usually extraparenchymal (90% of cases). Saccular aneurysms are the most frequent (up to 80%), and they appear to be related to arterial wall weakness at branch points secondary to discontinuity in the internal elastic lamina. The underlying etiologies are frequently atherosclerosis and fibromuscular dysplasia.9 Ehlers-Danlos syndrome (EDS) Type IV results in a high incidence of vascular lesions, and RAAs have been described.10
• False/pseudoaneurysms: do not include all layers of the artery. These can be extra- or intraparenchymal and can be secondary to blunt abdominal trauma, iatrogenic, dissection or can be mycotic or spontaneous.11,12

RAAs are usually asymptomatic and can be incidentally found with noninvasive imaging studies. Most patients (up to 90%) can be hypertensive. Hypertension can be related to the frequent association with renal stenosis, microembolization, compression of the main renal artery or its branches, or flow conditions.1 Infrequently, symptomatic RAAs can present with:

• Pain: some series have reported flank pain not related to rupture as the presentation form in 8–25% of patients.
• Urinary symptoms: hematuria can be present secondary to rupture of an intraparenchymal aneurysm into the calyces. Another rare presentation is a collecting system obstruction in large aneurysms.6
• Renal infarction: secondary to embolization from the aneurysm sac.
• Rupture: this is the most feared complication. It is uncommon (6,13 in males and non-pregnant women. There is no general consensus about the relation between aneurysm size and rupture risk, and therefore treatment threshold. Most authors have recommended asymptomatic RAA repair at diameters > 2 cm. However, rupture of an aneurysm of 1.5 cm diameter has been reported.1,7
• Aneurysm wall calcification is frequent (40%). It was associated with a lower rupture risk but, as there are reports of ruptured calcified aneurysms, the protective effect of calcification has been negated.
• General consensus exists regarding an increased rupture risk of RAAs during pregnancy. The hyperdynamic state, hormone-induced changes at the aneurysm wall and increased intra-abdominal pressure have been described as probable factors related to this increased risk during pregnancy. A maternal mortality rate of > 50% and fetal mortality of 85% have been reported.6,14

Most patients with RAAs can be conservatively managed. Contrast CT and gadolinium-enhanced MR are the preferred modalities for longitudinal follow-up. The most common and accepted indications for intervention are:1,9

• Diameter > 2 cm;

• Symptomatic RAA;

• RAA in pregnancy or anticipated pregnancy;

• Rupture;

• Expanding aneurysm.

In the case reported here, hip and back pain were very unspecific and probably not related to the presence of aneurysm in renal artery. So it was considered as an incidental RAA. In the absence of controlled data, controversy exists about management of asymptomatic and non-complicated RAAs. In the current case, considering aneurysm diameter and the association with distal severe stenosis and, after discussing with the patient and the referring physician, we decided to propose endovascular treatment. Surgery has been the standard intervention to treat RAAs. Different techniques are available and performed according aneurysm morphology and location. They include resection, aorto-renal bypass, patch angioplasty, extracorporeal vascular reconstruction with autotransplantation and nephrectomy.9,15 These techniques are complex and require a retroperitoneal approach. Reported complications include native renal branch or graft occlusion, global renal ischemia, ureteral stricture, distal embolization and systemic cardiovascular events in atherosclerotic aneurysms. These complications have accounted for a morbidity rate of approximately 30%.9 Technical advances and growing skill among specialists have allowed the endovascular approach to become a treatment alternative in patients with RAAs whose location imposes a challenging surgical approach, or in patients with high surgical risk. Different techniques and devices are available to treat RAAs and can be selected according to aneurysm type and location:

1. Aneurysm embolization:

• Coil embolization: is expanding its indication in different aneurysm locations as a result of the development of microcoils and better delivery catheters. These platinum or steel wires produce flow disturbances and secondary thrombosis, resulting in aneurysm exclusion. High technical success rates without significant complications have been reported. In a series of 12 patients with RAAs treated with selective coil embolization and followed for up to 2 years, successful and permanent occlusion of 11 aneurysms was achieved.16
• Stent-assisted coil embolization: as in other locations, saccular aneurysms can be treated by placing a stent across the neck and then filling the aneurysm with coils through its struts.17
• Onyx embolization: onyx is a mixture of ethylene-vinyl alcohol copolymer (EVOH) dissolved in dimethyl sulfoxide (DMSO) opacified with tantalum powder. When it comes in contact with blood, a rapid diffusion of DMSO solvent produces EVOH precipitation and solidification. This substance is delivered to the aneurysm through a microcatheter once the neck of the aneurysm is temporally occluded by a balloon. Most of the experience with its use arises from endovascular treatment of cerebral aneurysms and arteriovenous malformations. The main limitations of embolization techniques include the risk of late recanalization, coil migration or non-target embolization when solutions are used. Suboptimal results may occur when treating wide-necked aneurysms with this technique, even with stent-assisted embolization.9

2. Stent-grafts: these have been used to treat different pathologies including occlusive disease, aneurysms, arteriovenous fistulae, dissection, rupture and trauma.18 When placed across the aneurysm neck, stent-grafts produce direct sealing and aneurysmal occlusion. These are metal stents lined with PTFE or Gore-Tex that can be used to treat saccular or fusiform aneurysms. Their use requires a segment of normal artery proximal and distal to the aneurysm. When, as in the case presented here, there is an association of aneurysm and stenosis, stent-grafts provide the ability to treat both conditions. The main limitation of these devices includes side-branch occlusion in lesions located at a bifurcation. Also, the short length of the vascular bed can produce support difficulties when trying to advance and place the device in mid or distal segments of the main renal artery. Several devices are now commercially available with lower profiles. They can be classified according to their delivery system:

• Self-expandable stent-grafts: due to possible jumping and shortening during deployment, this kind of prosthesis is not used for lesions that require precise stent positioning. Moreover, the lower radial force makes self-expandable stents less appropriate to treat tight and calcified lesions like the severe stenosis distal to the aneurysm in the case discussed here.
• Balloon-expandable stent-grafts: when precise stent positioning and radial force are needed, this kind of device is preferred over self-expandable stent-grafts. Many case reports and series have reported a high technical success rate when treating with a balloon-expandable covered stent for different pathologies such as atheromatous lesions, in-stent restenosis, aneurysms, dissections and stent fractures.18–20 We selected the ADVANTA V12 device (Atrium Interventional Surgery, Hudson, New Hampshire), which is a stainless steel stent covered with microporous PTFE. Stent diameters of 5–10 mm are 6 and 7 Fr compatible and 12, 14 and 16 mm diameters are 9 and 11 Fr compatible. As discussed previously in the case presented here, the short length of the vascular bed produced support difficulties when trying to advance the device. This problem was overcome by placing an Amplatz super-stiff wire and by advancing a 7 Fr sheath to the mid portion of the renal artery. The long-term patency of stent-grafts, specifically in the renal vasculature, remains unknown. Data can be extrapolated from trials that tested the longitudinal function of these devices in other vascular territories. The COBEST trial presented at LINC 2010 and not yet published, reported a 95.4% freedom of restenosis at 18 months in patients with iliac occlusive vessel disease treated with the Advanta V12 stent. Other experience with this device in iliac disease has shown a primary patency rate of 91.1% at 1 year.22 Specifically in the renal vascular bed, the Atrium iCast stent has shown a primary patency rate of 92% at 6 months and 72% at 12 months.19 In the case presented here, follow-up with CT angiography showed that treatment with a stent-graft produced durable results, with aneurysm exclusion and absence of significant restenosis at 2 years.

Conclusions

Endovascular techniques are continuously expanding. Depending on their anatomical characteristics, RAAs can be treated with different modalities. Stent-graft placement was demonstrated in the present case to be an effective and durable treatment option. Careful planning of the procedure and close surveillance of complications are important keys to consider.

Acknowledgment. The authors wish to thank Dr. Adolfo Lopez Campanher for his assistance in preparing the case history.

References

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17. Clark TW, Sankin A, Becske T, et al. Stent-assisted Gugliemi detachable coil repair of wide-necked renal artery aneurysm using 3-D angiography. Vasc Endovascular Surg 2007;41:528–532.

18. Gaxotte V, Laurens B, Haulon S, et al. Multicenter trial of the Jostent balloon-expandable stent-graft in renal and iliac artery lesions. J Endovasc Ther 2003;10:361–365.

19. Giles H, Lesar C, Erdoes L, et al. Balloon-expandable covered stent therapy of complex endovascular pathology. Ann Vasc Surg 2008;22:762–768. Epub 2008 Oct 15.

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21. Axelrod DJ, Freeman H, Pukin L, et al. Guide wire perforation leading to fatal perirenal hemorrhage from transcortical collaterals after renal artery stent placement. J Vasc Interv Radiol 2004;15:985–987.

22. Bosiers M, Iyer V, Deloose K, et al. Flemish experience using the Advanta V12 stent-graft for the treatment of iliac artery occlusive disease. J Cardiovasc Surg (Torino) 2007;48:7–12.

_______________________________________________________________________

From the Interventional Cardiology Department, Instituto de Cardiología de Corrientes “Juana F. Cabral”, Corrientes. Argentina. The authors report no financial relationships or conflicts of interest regarding the content herein. Address for correspondence: Marcelo A. Aguero, MD, Interventional Cardiology Department, Instituto de Cardiología de Corrientes “Juana F. Cabral”, Bolívar 1334. Corrientes. Argentina. E-mail: marceloaguer@gmail.com>

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