Renal artery stenosis stenting with unmasking and embolisation of a renal arteriovenous fistula

Abstract

A man in his 70s was presented to the emergency department with uncontrollable hypertension and worsening renal function on a background of atherosclerosis-related bilateral renal artery stenosis. Following progressive deterioration in renal function and refractory hypertension, the patient was referred to interventional radiology for consideration of renal artery stenting. Following stenting of the right renal artery, a large renal arteriovenous fistula became apparent, which required emergent embolisation. Both procedures were successful, with excellent clinical and radiological responses.

Background

Atherosclerosis is the most common cause of renal artery stenosis (RAS), estimated to be the causative factor in over 90% of cases.¹ Atherosclerosis-related RAS classically involves the renal artery ostia and the proximal one-third of the artery.¹ Treatment options include medical therapy and revascularisation, with percutaneous stenting being the preferred approach to revascularisation.² Indications for revascularisation include unexplained heart failure and pulmonary oedema, hypertension considered to be refractory to medical therapies, and rapidly declining renal function.³

A renal arteriovenous fistula (RAVF) is an uncommon vascular anomaly defined as an abnormal direct communication between an artery and vein within the kidney. Acquired RAVF is estimated to make up 70% of cases, with percutaneous biopsy/intervention being a classic cause.⁴ Congenital and idiopathic categories comprise the remaining cases, making up 25% and 3–5%, respectively.⁴ Although small lesions are often asymptomatic, common clinical manifestations of larger lesions include hypertension, high-output cardiac failure and gross haematuria.⁵

We report an interesting case of RAS stenting with subsequent unmasking and embolisation of a RAVF.

Case presentation

A man in his 70s was presented to the emergency department with severe hypertension (212/94 mm Hg) and worsening renal function on a background of bilateral RAS. Additional relevant medical history included hypertension, dyslipidaemia, chronic kidney disease (CKD) and heart failure with preserved ejection fraction. A significant smoking history was noted. During the months prior to this presentation, blood pressure was relatively well controlled with medical therapy, while renal function was slowly worsening. Following admission, there was progressive deterioration of renal function, which required intermittent haemodialysis. The patient remained hypertensive despite being on six antihypertensive medications, including intravenous labetalol. This prompted a referral to the interventional radiology (IR) team for consideration of percutaneous renal artery stenting.

Investigations

Six months prior to this presentation, the patient had undergone a CT angiogram of the renal arteries. This demonstrated bilateral RAS with near-complete occlusion of the proximal right renal artery. The right kidney was normal in size; the left kidney was reduced in size and likely provided limited function.

At the time of referral to IR, the average blood pressure reading was 198/96 mm Hg, the serum creatinine was 727 umol/L and the patient was anuric. The patient was also noted to have macroscopic haematuria, for which a cause had not been identified.

Treatment

Following a multidisciplinary team discussion, it was felt that the patient met criteria for percutaneous renal artery stenting and that this would be the most appropriate intervention. This was discussed in detail with the patient, and written informed consent was obtained. Given the reduced size of the left kidney and likely reduced function, a decision was made to initially stent the right renal artery.

The initial aortogram demonstrated bilateral RAS. Diagnostic angiography at the ostium of the right renal artery demonstrated near-occlusive calcific stenosis just beyond the ostium with slow flow through the vessel (figure 1). At this stage, a subtle vascular abnormality at the interpolar region/upper pole was also noted (figure 2). A 6 mm × 22 mm atrium-covered V12 stent was deployed over the stenosis and sequential 6 and 7 mm balloon angioplasty of the stent was performed. Excellent angiographic response was demonstrated on completion of the angiography, with prompt blood flow through the right renal artery (figure 3).

Figure 1.

Digital subtraction angiogram of the right renal artery demonstrating near-occlusive stenosis just beyond the ostium.

Figure 2.

Digital subtraction angiography demonstrating a subtle vascular abnormality at the interpolar region/upper pole indicated by an arrow.

Figure 3.

Digital subtraction angiography of the right renal artery following stent placement.

The previously seen subtle abnormality in the right interpolar region/upper pole became much more pronounced following successful revascularisation. Angiography confirmed this to be a arteriovenous fistula involving peripheral vessels in the interpolar region/upper pole of the right kidney (figure 4). This was catheterised and coil embolised using multiple 2 mm (2 mm × 2 cm, 2 mm × 4 cm) and 3 mm (3 mm × 15 cm) platinum detachable coils (Ruby, Penumbra, Alameda, CA, USA). Angiography at the end of the procedure demonstrated complete occlusion of the arteriovenous fistula (figure 5).

Figure 4.

Digital subtraction angiography of the right renal artery following stent placement showing a large renal arteriovenous fistula at the interpolar region/upper pole (arrow) which has significantly increased in size when compared with the prestenting angiogram.

Figure 5.

Digital subtraction angiography of the right renal artery demonstrating near-complete occlusion of the renal arteriovenous fistula following placement of multiple Ruby coils.

Outcome and follow-up

The patient was reviewed on the ward 1 day postprocedure. At this point, blood pressure had improved, measuring 161/50 mm Hg. Urine output had increased to 150 mL/hour and the macroscopic haematuria had completely resolved. Serum creatinine was largely unchanged at 717 umol/L, which was to be expected at this early postprocedural stage.

The patient was discharged home 4 weeks following the procedure. Prior to discharge, urine output was within normal limits, and serum creatinine had decreased to 154 umol/L. Renal function was stable and classified as CKD 3a/b by the renal team. Blood pressure was well controlled at 134/66 mm Hg on just two antihypertension medications. There was a history of oligoanuric acute kidney injury with the introduction of angiotensin-converting-enzyme inhibitor/angiotensin receptor blocker (ARB). Stenting allowed the patient to safely tolerate an ARB, which will offer significant cardiovascular health benefits. Overall, the patient had an excellent response, both clinically and radiologically. The patient will be closely followed by the renal team as an outpatient to establish a long-term response.

Discussion

We present a complex case involving concomitant RAS and RAVF with demasking and increased flow through RAVF following renal artery stenting, necessitating emergency embolisation.

Atherosclerosis represents the most common cause of RAS, making up more than 90% of cases.¹ Risk factors for atherosclerosis-related RAS are identical to those for atherosclerotic disease elsewhere in the body and include hypertension, dyslipidaemia and tobacco smoking, all of which were present in our case. Atherosclerosis-related RAS classically involves the ostium and proximal one-third of the vessel. These findings are clearly demonstrated on imaging modalities such as CT angiography, MR angiography and digital subtraction angiography, which is considered the current gold standard. A unilaterally small or atrophic kidney is commonly seen when disease is dominant on one side. This asymmetry in size often indicates functional capacity and can determine the most promising target for revascularisation, as demonstrated in our case. Typical imaging appearances were present in our case, with near-complete occlusion of the right renal artery ostium and marked asymmetry in kidney size.

RAVF is an uncommon vascular anomaly defined as an abnormal direct connection between an artery and vein within the kidney. RAVF can be classified as acquired, congenital or idiopathic.⁶ Acquired RAVF accounts for 70% of cases and can occur secondary to percutaneous renal biopsy, trauma, surgery, inflammatory conditions or malignancy. Percutaneous renal biopsy is the most common of these with a reported post-biopsy incidence of 3–5% in native kidneys and 10–16% in transplant kidneys. Of the remaining cases, congenital causes make up 20% and idiopathic 3–5%. Interestingly, no acquired cause was identifiable in our case, raising questions about the aetiology.

While the vast majority of small RAVF are asymptomatic, large high-flow lesions are often symptomatic. Common clinical manifestations include high-output cardiac failure, hypertension, reduced renal function and macroscopic haematuria.⁵ All of these features were present in our case. It is worth mentioning that, with the exception of macroscopic haematuria, there is significant overlap in clinical features between RAS and RAVF, which can create uncertainty in determining the disease process responsible for individual signs and symptoms when both conditions are present. The macroscopic haematuria noted in our case was likely directly attributable to the RAVF, given the complete resolution following embolisation. The remaining clinical features were felt to be secondary to RAS.

Indications for RAVF treatment include recurrent or persistent haematuria, increasing fistula size, hypertension and high-output cardiac failure.⁴ Historically, open surgery, often entailing partial or total nephrectomy, was the standard treatment. Embolisation is now the preferred treatment option, offering a lower complication rate and the ability to preserve renal function, with surgical treatment reserved for larger lesions and for those that have failed embolisation.⁷ Multidisciplinary team discussion is essential to determine the most suitable treatment option. Our case provides a unique scenario as the RAVF only became accurately apparent following revascularisation. The subsequent rapid increase in size was felt to warrant emergency embolisation.

A similar case to ours was reported in 1995,⁸ describing a concomitant RAS and RAVF in an allograft with rapid enlargement of the RAVF following revascularisation. Treatment with embolisation and subsequent surgical repair was unsuccessful, and the allograft ultimately failed. To the best of our knowledge, we present the first case of concomitant RAS and RAFV in a native kidney with successful RAVF embolisation.

Learning points.

• Stenting for renal artery stenosis represents an effective treatment option for a select patient cohort, as demonstrated in our case.

• A multidisciplinary team approach is vital to determine patient suitability for the procedure.

• We present an unusual case of successful renal artery stenting with unmasking and embolisation of a renal arteriovenous fistula.

Ethics statements

Patient consent for publication

Consent obtained directly from patient(s)