Successful Endovascular Renal Artery Aneurysm Exclusion Using
the Venture‚Ñ¢ Catheter and Covered Stent Implantation: A Case Repo

Recent advances in balloon and stent technology have increased procedural success rates have resulted in expanded indications for percutaneous treatment of complex peripheral arterial disease. As a consequence, lesions traditionally approached with a surgical strategy, such as those involving the renal arterial system, are currently more often treated with percutaneous techniques.¹ Despite these advances, certain anatomical settings, such as extreme vessel angulation or tortuosity, may make lesion access difficult.

The availability of new steerable devices, like the Venture^™ Wire Control Catheter (St. Jude Medical, Inc., St. Paul, Minnesota), could assist in challenging cases where conventional techniques have failed either due to poor backup support or imprecise wire control. Possible additional benefits are reductions in procedure time, radiation exposure, contrast load and costs.

We report our experience of the successful percutaneous treatment of a renal artery aneurysm (RAA) in a young male using the Venture catheter to selectively engage the aneurysm and implant a balloon-expandable covered stent for its exclusion.

Case Report

Clinical presentation and angiographic findings. A 46-year-old male presented with accelerated/malignant hypertension, a 3-day history of macroscopic hematuria and left-sided lower back pain. The patient was a current smoker, with no previous history of cocaine or other drug abuse, and a positive family history for coronary artery disease. Six months earlier, he was admitted to another hospital for back pain with no associated hematuria. Blood pressure values at that time were 140/90 mmHg. Ultrasound imaging did not show any pathological findings, however, the patient was diagnosed as having renal colic, which was successfully treated with antispasmodic and pain-relieving drugs. Antibiotic therapy (levofloxacin 500 mg daily) was also prescribed for 5 days.

One month later, the patient was admitted to another hospital for chest pain. Blood pressure values on that occasion were 190/120 mmHg; intravenous clonidine and diuretics were administered. Electrocardiography (ECG) and echocardiography did not show any pathological finding (ejection fraction 60%), and no significant coronary artery disease was detected angiographically. There were no pathological findings, but a 10 mm calcific image, located near the portal vein and diagnosed as possible choledocolithiasis or renal cyst, was reported by abdominal computed tomography scan. The patient was discharged on a dihydropiridine calcium channel-blocker (nifedipine 30 mg daily), a diuretic (amiloride/ hydroclorothiazide 100 mg daily), an angiotensin-converting enzyme inhibitor (enalapril 20 mg daily) and aspirin.

Despite full compliance with medications, optimal blood pressure control was never achieved, and the patient’s blood pressure values remained around 160/110 mmHg. Technetium (Tc)- 99m diethylenediaminepentaacetic acid (DTPA) scintigraphy showed normal kidney size and morphology, left kidney ectatic renal calyces, delayed peak/excretion phase and hypoperfusion of the left kidney, which accounted for 62% of total renal function. These findings were interpreted as the outcome of chronic pyelonephritis. Several laboratory tests were performed in the following months (to assess renal, thyroid and hepatic function, coagulation, homocysteine and CRP concentration, autoantibodies presence, etc). All results were normal, except the patient’s serum renin and aldosterone levels, which were elevated.

The patient’s blood pressure on admission was 190/130 mmHg. Physical examination was unremarkable; the patient was apyrexial and no bruits were present on his flanks. His serum creatinine concentration was in the normal range (1.2 mg/dL). Abdominal ultrasonography excluded the presence of an abdominal aortic aneurysm and suggested a dilated left renal artery.

The patient underwent selective renal angiography via the right femoral artery, which demonstrated a sacciform aneurysm of approximately 1.5 cm diameter arising from the first segmental branch of the left main renal artery (Type I renal aneurysm).² This side branch originated from the main renal artery with a 90 degree take-off (Figure 1) and immediately before the aneurysm sac origin. Its caliber was significantly reduced by a 90% diameter stenosis (Figure 1A, arrow). The remainder of the renal vascular system appeared normal. In light of the patient’s malignant hypertension in conjunction with left-sided back pain (possibly suggesting impending rupture) and the size of the aneurysm, we decided to proceed with a percutaneous approach in order to exclude the aneurysm and treat the stenosis.

Treatment. After administration of 100 UI/Kg heparin, the main left renal artery was engaged with a 6 Fr renal guiding catheter. Several unsuccessful attempts using different 0.014 inch wire types with increasing weight (Balance medium weight, Abbott Vascular Devices, Redwood City, California/Guidant, Santa Clara, California; Rinato Wire, Asahi Intech, Japan; Intermediate ACS, Asahi Intech; and Pilot 50, Abbott Vascular Devices/Guidant), and reshaped with different bends, were made to selectively wire the side branch vessel. Wire crossing proved extremely difficult due to the angulated side branch takeoff. Moreover, despite initial success in engaging the side branch origin on some occasions, the wire prolapsed down the main renal artery immediately after a steering force was applied in order to cross the tight stenosis. At this point we decided to use the Venture catheter to provide wire-steering control and improve pushability. The Venture catheter was advanced over a Balance mediumweight 0.014 inch wire, offering excellent wire backup support (Figure 2, insert) and allowing wire steering inside the aneurysm sac.

The Venture catheter was then further advanced, and 5 mLof contrast media was injected through it to selectively opacify the sac in order to rule out the presence of efferent vessels (Figure 2). Once the absence of efferent vessel was confirmed, a 6.0 x 16 mm Jostent peripheral stent graft (Jomed, Helsingborg, Sweden) was implanted. The stent was deployed under roadmap guidance precisely at the origin of the side branch site of the aneurysm and fully expanded by balloon inflation at 10 atm (Figure 3). The final angiogram demonstrated complete aneurysm exclusion and resolution of the subocclusive stenosis, with preserved patency of the remaining segmental branches of the renal artery, none of which were feeding the aneurysmal sac (Figure 4).

Outcome. The patient’s postprocedural course was uneventful. He was discharged 2 days after admission, asymptomatic and with normal renal function (serum creatinine concentration at discharge was 0.85 mg/dL). His blood pressure values at discharge were 137/90 mmHg.

Clopidogrel (75 mg/day) and aspirin (100 mg/day) therapy were recommended for 4 weeks, after which long-term aspirin therapy was prescribed. Antihypertensive therapy at discharge consisted of a dihydropiridine calcium channel-blocker (lecarnidipine 20 mg daily) and an angiotensin II receptor-blocker (losartan 25 mg daily). Close blood pressure and renal function monitoring and follow-up renal duplex studies at 1-month, then 6-month intervals were recommended.

At 20 months, the patient remains symptom-free, with normal blood pressure (24-hour noninvasive blood pressure monitoring performed 10 months after the procedure showed mean blood pressure values of 130/86 mmHg), and takes aspirin 100 mg daily, an angiotensin-converting enzyme inhibitor (ramipril 10 mg daily), a different dihydropiridine calcium channelblocker (amlodipine 10 mg daily) and an alfa receptor-blocker (doxazosin 2 mg daily). No change in renal function occurred (creatinine 0.86 mg/dL). Renal duplex sonography obtained at 4, 8, 14 and 20 months after stent placement showed a widely patent renal artery, normal renal perfusion and complete aneurysm exclusion.

Discussion

Renal artery aneurysms. RAAs are uncommon vascular anomalies, with a reported prevalence in the general population of 0.01%–1%.^3,4 They are the fourth most common visceral artery aneurysm after splenic, hepatic and superior mesenteric artery aneurysms, and account for approximately 25% of visceral aneurysms.⁵

In comparison with renal artery occlusive disease, they are more likely to affect younger patients, often without significant atherosclerotic risk factors. Tham et al⁶ reported in an angiographic case series, including all the RAAs found during 8,525 renal angiographies, a higher prevalence of RAAs in men (53 versus 47%). Recent reports, conversely, indicate a higher prevalence of RAAs in women.⁷ This might be related to the more frequent occurrence in women of fibromuscular dysplasia, which is the vascular disease most often (in 34–51% of cases) associated with RAAs.^8,9

Both the natural history and the clinical significance of RAAs remain uncertain, consequently, the indications for theirmanagement are controversial.⁶ Most RAAs remain free of clinical signs and symptoms, and therefore are usually detected during imaging examinations performed for other indications.

The risk of rupture and the possibility of embolization, which may cause hematuria, flank pain, renal function deterioration and eventual renal infarction, are often proposed as the rationale for RAA treatment.^6,10 Even though rupture is often associated with devastating consequences, the actual risk of rupture appears to be low (about 5%).¹¹

The possible contribution of RAAs to secondary hypertension may be another indication for therapeutic intervention. ^5,9,12 Actually, RAAs are associated with hypertension, either poorly or nonresponsive to medications, in up to 70–80% of cases.^8,9,13

The potential causative mechanisms of secondary hypertension related to RAA are still unclear.³ Several theories such as mechanical kinking or twisting of the renal artery causing impaired blood flow, segmental parenchymal ischemia due to microembolization, flow turbulence or coexistent renal artery stenosis, may explain this relationship via a renin-mediated mechanism.⁸ The incidence of hypertension associated with RAAs is actually higher in patients with associated renal artery stenosis;⁹ however, the blood pressure response and the reduction in antihypertensive medications appear similar in patients treated for RAA and stenosis and those without coexisting renal artery stenosis.⁸

Accordingly, English et al¹³ reported on the surgical outcome of 62 patients treated for RAAs, 89% of whom had hypertension, while only 22% had coexisting renal artery stenosis. Despite this, the majority of hypertensive patients (75%) experienced beneficial blood pressure response at a mean follow up of 48 months after RAA repair, including 21% who became normotensive off all medications.

Other surgical series report similar rates of improvement in hypertension following RAA treatment in conjunction with fewer antihypertensive medications^8,14 In view of the short hypertensive history and of the contemporary treatment of the coexisting renal artery stenosis, a certain improvement in hypertension after RAA exclusion was expected in our patient. Nevertheless, no reliable parameters to predict whether a patient with RAA will be cured from hypertension after successful RAA treatment are available to date.

Selection criteria for the treatment of RAAs have usually correlated patient characteristics and anatomic features of the aneurysm to its risk of rupture. Young pregnant females, especially in the third trimester of pregnancy, have been considered to be at the highest risk for rupture. It is estimated that approximately 80% of women with preexisting RAA will experience rupture during pregnancy, with high associated mortality rates for both mother and fetus. Both the hemodynamic changes (increased cardiac output and blood pressure) and the hormonal alterations affecting the arterial wall may play a role.^15,16 Other factors predisposing patients to rupture are the presence of polyarteritis nodosa or fibromuscular dysplasia.^17,18

On the other hand, some authors have considered the RAA size as the only crucial criterion for its treatment. Intervention is recommended for RAAs > 1.0 cm when hypertension is present, and for RAAs between 1.5 to 2.0 cm when no hypertension is present.^19–21 Conversely, fusiform shape and calcification have been suggested as protective against rupture; however, several series have demonstrated no correlation between these characteristics and rupture risk.^22,23

Notwithstanding the size thresholds for RAA treatment, there are some reports of conservative management.^6,8,19 However, a size of > 2 cm portends the highest risk of RAA rupture, therefore close follow-up surveillance by computed tomography, ultrasound or magnetic resonance imaging to detect any increase in RAA size is recommended.¹³

Approaches for RAA treatment. Although the diagnosis is often made incidentally, arteriography is essential for good operative planning. Three general approaches have been described for RAA treatment: (1) surgery with either in situ aneurysmectomy and bypass with an autologous conduit, or nephrectomy;^5,14 (2) transcatheter embolization,^24–26 particularly useful for the management of life-threatening hemorrhage; or (3) endovascular exclusion by stent graft.^2,27,28

The angiographic pattern of the RAA and its feeding artery or arteries help to determine the optimal method of treatment. In this setting, Rundback et al² described three main types of RAAs: saccular RAAs arising from either the main renal artery or a large segmental branch (Type 1), which are the most common; fusiform aneurysms (Type 2); and intralobar aneurysms (Type 3), which arise from small segmental arteries that supply a limited portion of the renal parenchyma.

Type 1 RAAs can be successfully treated with stent graft implantation; Type 2 RAAs are best treated by a surgical approach, while Type 3 RAAs may be treated with catheterdirected embolization using microcoils.

The surgical treatment of RAAs, considered the gold standard therapy, is currently performed according to one of the following options:

a) aneurysmectomy and renal artery branch repair, performed either in situ (with the least risk of kidney damage) or ex vivo (especially for complex distal RAAs involving several renal artery branches, with associated longer renal ischemia times);

b) renal bypass surgery (with either autologous or PFTE conduits) with exclusion of the aneurysm; and

c) nephrectomy.

These are, however, major and technically demanding surgical procedures, with reported morbidity rates of up to 28%^11,14,29 and prolonged recovery periods. Aside from abscess, bleeding and wound infection, possible complications include death, need for nephrectomy, early or (approximately 10% of cases) delayed graft occlusion⁸ and branch artery stenosis or occlusion after aneurysm resection, which may require further aorto-renal bypass.⁹ Recently, laparoscopic surgery has been proposed as a possible minimally invasive alternative to open surgical RAA repair.^30,31

The percutaneous treatment of RAAs, increasingly accept-ed as safe and effective, offers several advantages compared to traditional surgical therapy due to its minimal invasiveness. It avoids the risk of general anesthesia and minimizes renal ischemic time. The patient’s recovery is more rapid and the hospital stay is shorter. There is, furthermore, the possibility of repeating the procedure in the event of incomplete aneurysm exclusion and, should the endovascular treatment not be feasible or successful, surgical intervention is not ruled out. In addition, the endovascular technique could be of particular value in the treatment of those RAAs located in a solitary kidney, since in almost all surgical series, there is a certain rate (up to 5%)⁸ of unplanned nephrectomy procedures secondary to technical complications. In one of the largest experiences using transcatheter embolization, Klein et al²⁶ successfully treated 12 RAAs with microcoils. The RAAs treated in this series were located within the main renal artery (2 cases), within the primary division of the main renal artery (8 cases), or were intrarenal (2 cases).

With regard to the exclusion of RAAs by endovascular grafts, several cases performed either with prefabricated covered stents^{18,28,32–41} or with “homemade” PTFE-covered^2,27 or autologous vein-covered⁴² stent grafts are reported in the literature(Table). Collectively, these data support the feasibility of this approach for RAA treatment in experienced hands.

In addition, percutaneous treatment with covered stents may be a safe therapeutic alternative to surgery in those cases with an appropriate artery caliber proximal and distal to the aneurysm, and with the aneurysm neck located along the renal artery not close to a branching point. Moreover, this approach offers the option of excluding the aneurysm and at the same time treating a coexisting renal artery stenosis,^18,27,33,40 as in the present case.

A possible reported complication is the occlusion of a renal branch after stent deployment.^2,32,34,36 Sacrifice of branch vessels can occur mainly when treating an aneurysm located at a branch point, with concomitant loss of renal mass, significant patient discomfort and prolongation of hospital stay.³² Some authors³³ have indeed contraindicated the stent graft approach when the RAA is located close to a bifurcation. Deployment of a bifurcated covered stent via the double-wire technique might be a solution for treating such lesions. Another complication reported in the literature is the occlusion of the main renal artery soon after stent graft deployment, which in one case was treated with local thrombolysis,⁴¹ and in the other, with additional stent implantation associated with local thrombolysis.²

In the present case, the option of stent graft placement was chosen not only due to the RAA anatomic features and the side branch stenosis, but also because coil embolization of an important vessel may result in non-target embolization or migration of the coils or delayed recanalization of the aneurysm.

The complexity of anatomy offered an additional technical challenge in our case. The Venture catheter was extremely useful in allowing engagement of the angulated take-off side vessel and in providing excellent wire backup for lesion crossing. Scenarios similar to this one, with extreme angulation of the side branch ostium, are not uncommon. A combination of over-the-wire balloons or different guiding catheters may enhance backup, or different guidewires may be tried in the attempt to improve steerability. However, in the presence of extreme angulation, conventional techniques may be unsuccessful in lesion negotiation.

The Venture is a low-profile 6 Fr compatible flexible guiding catheter with an 8 mm deflectable atraumatic radioopaque distal tip (Figure 5). The tip can be moved, supporting and orientating the wire toward any angle between 0 and 90 degrees by rotation of a control knob located on the proximal handle (Figure 6, Panels A–C). This innovative mechanism improves wire steerage through challenging lesions, while preserving or even increasing pushability. Furthermore, the over-the-wire shaft accommodates any 0.014 inch guidewire, and also allows wire exchange if needed.

Experience with endovascular stenting, to date, is limited to Type 1 RAA aneurysms. The Venture catheter may also make the percutaneous approach a treatment option for Type 2 RAAs that are traditionally considered for surgery only because of the angulation at the junction of the aneurysm with the distal artery.

An important limiting factor in the use of covered stents is the presence of small-caliber and tortuous renal vessels, where the delivery of a covered stent may be technically unattainable because of existing device limitations. Improvement of the profile and longitudinal flexibility of these stents, thereby facilitating positioning and deployment even in complex lesions, is warranted. In addition, although reports have shown persistent RAA exclusion with wide patent renal arteries up to 24 months after stent implantation,³³ long-term stent graft patency remains uncertain.³⁵ From this perspective, this technique may not be the best option when treating younger patients. Therefore, careful follow-up imaging is mandatory to assess the long-term outcome of this percutaneous approach for RAA treatment. Saltzberg et al recommend 1-month, 6-month and then yearly surveillance with either contrast CT scan or ultrasound.³⁷ Follow-up imaging may aid in the detection of early or delayed recurrence, endoleak, end-organ ischemia or stent migration. In addition, since up to 29% of RAAs could be bilateral,¹³ follow-up imaging may detect the development of a contralateral RAA.

Conclusions

The present case demonstrates the efficacy and safety of the percutaneous approach in treating RAAs, even in the presence of a complex anatomy. The Venture catheter might make the percutaneous approach an option in the treatment of Type 2 RAAs traditionally considered for surgery.

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