Skip to main content

Advertisement

ADVERTISEMENT

Review

Renal Artery Intervention: Endovascular Techniques

February 2011
2152-4343

Abstract

Significant renal artery stenosis (RAS) may result in deterioration of arterial hypertension and/or renal insufficiency and may contribute to cardiovascular diseases such as diastolic and systolic heart failure. Percutaneous transluminal angioplasty (PTA) is the established therapy for RAS of fibromuscular disease origin. The role of cutting balloon angioplasty in this indication still needs to be investigated. In atherosclerotic RAS, stenting has shown superior acute and long-term technical outcomes compared to PTA. Technical improvements such as dedicated guiding catheters, the downsizing of devices including wires, balloon catheters and stents, made the intervention more successful and safer. Numerous single-center studies have reported the beneficial effects of percutaneous revascularization of RAS of different etiologies. Even if the recent randomized STAR and ASTRAL trials did not show any benefit of RAS revascularization over medical therapy, there is nonetheless evidence that stenting of hemodynamically relevant atherosclerotic RAS has an impact on blood pressure control, renal function and left ventricular hypertrophy. This article introduces interventional treatment techniques step-by-step.

VASCULAR DISEASE MANAGEMENT 2011;8(2):E21–E27

Key words: renal artery stenosis; angioplasty; stent; technical outcome

Historical Background

The first renal artery balloon angioplasties were performed by Felix Mahler in Berne and by Andreas Grüentzig in Zurich in 1977. Balloon angioplasty of renal artery stenosis (RAS) of fibromuscular disease nature yields satisfying acute and long-term results with procedural success rates of 82–100% and restenosis rates of about 10%.1–5 However, balloon angioplasty of ostial atherosclerotic lesions was limited by a low acute technical success rate of 50–62% and a high restenosis rate of up to 47% in the long-term due to dissections, elastic recoil and rigidity of the lesion.1,6 Stenting has revolutionized percutaneous renal revascularization. Two randomized studies demonstrated superior technical outcomes of stenting over balloon angioplasty1,7 in the treatment of atherosclerotic ostial RAS, the most common manifestation of RAS. Nowadays, using premounted low-profile stent devices, atherosclerotic RAS can be treated successfully in almost all cases, with restenosis rates ranging from 3–23% depending on the definition of restenosis and the diameter of the renal artery.7–11

Morphology and Pathophysiology

Atherosclerosis accounts for approximately 90% of the cases of RAS. The prevalence of atherosclerotic RAS increases with age, particularly in patients with diabetes mellitus, hyperlipidemia, diffuse types of peripheral occlusive disease, coronary artery disease or hypertension.12,13 Atherosclerotic RAS is most often caused by plaque formation in the aortic wall, with progression into the renal artery origin, resulting in the typical appearance of the eccentric ostial atherosclerotic RAS (Figure 1), and resulting in specific peri-interventional risks such as atheroembolism. Atherosclerotic RAS is a progressive disease, even in initially unaffected arteries, with an up to 18% occlusion rate within 1 year.14–17 A close association between severity of RAS and kidney atrophy and ischemic nephropathy is reported.18,19 However, the exact etiology of the development of ischemic nephropathy is still uncertain.20 The second frequent aetiology of RAS, fibromuscular dysplasia (FMD), is a collection of vascular diseases that affects the three layers of the arterial vessel wall: intima, media and adventitia, and is of unknown etiology. FMD accounts for 20,21 Inflammatory diseases (e.g., Takayasu arteritis) and external compression are rare conditions resulting in RAS.

Renal Artery Revascularization Techniques

Arterial access Femoral approach. Femoral access is established as a standard approach for renal interventions, with few exceptions such as untreated severe stenosis/occlusion of the pelvic arteries or abdominal aorta, severe kinking of the pelvic arteries or an acute angle of the renal artery. The “guiding catheter technique” requires a 6 or 7 Fr sheath with a hemostatic valve with a length of 11 cm (various manufacturers, e.g., Avanti™, Cordis Corp., Miami Lakes, Florida, or Terumo Corp., Leuven, Belgium). In tortuous iliac arteries, the use of a longer sheath (23 cm, various manufacturers) for better manipulation of catheters and wires can be helpful. Alternatively, a preshaped long sheath (Vista Britetip IG™ Cordis; Destination®, Terumo) can be used. Hereby, the device diameter is downsized by 1 Fr (5 Fr instead of 6 Fr), and the risk of access-site complications may be reduced by the expense of a less exact orientation of the preshaped tip. Brachial approach. The left brachial access is the preferred access because no brain-providing artery, except the left vertebral artery, must be passed with a wire or catheter. A ≤ 6 Fr common or a 7 Fr sheath is introduced into the brachial artery in the fossa antecubitalis using a micropuncture set. As for the femoral approach, the use of a guiding catheter (90 cm length) is recommended. Mostly, catheter types used are the “right Judkins 4”, the “right Amplatz 1”, and the “multipurpose” (various companies). Alternatively, a 90 cm long, straight 6 Fr sheath (Cook, 4632 Bjaeverskov, Denmark) or a multipurpose shaped guiding sheath (Vista Britetip IG™) can be positioned proximal to the origin of the renal artery.

Renal artery angiography

In a non-tortuous aorta, the origins of right and left renal arteries are identified best in a 20° left anterior oblique (LAO) projection (Figures 2A and B). Semiselective and selective baseline angiograms should be performed to determine the optimal projection for the intervention. Conventional angiography sometimes allows better visualization of the lesion, and the anatomy compared to DSA-technique because of potential movement artifacts of DSA. Prior to the first selective renal angiography, the guiding catheter should be cleaned from debris by passive back-bleeding or active aspiration of 10 cc of blood via a Y-connector (“proximal protection”, Figure 3). This technique reduces the risk of renal embolism.

Technique of renal artery stenting

For the femoral approach a variety of guiding catheter configurations such as “renal double curve, RDC”, “hockey stick”, “right Amplatz, AR-1”, “right Judkins, JR-4” or “IMA” are available to guarantee a stable position proximal to the renal artery origin. The guiding catheter technique is the fastest technique with the lowest intervention and radiation time. After placing the guiding catheter close to the renal artery origin, a steerable stiff 0.014-inch guidewire with a flexible tip should be used to cross the lesion. Some authors, like Feldman et al22 recommend a so-called “no-touch technique” (Figures 4 A–D) that needs upsizing of the guiding catheter by 1 Fr. Coming from the femoral access, it can become difficult to even introduce a guidewire into the renal arteries with an acutely angled off-take. The telescoping technique can solve this access problem. The renal artery orifice can be cannulated with a 5 Fr SOS-Omni Soft-Vu-catheter™ (Angio Dynamics, Inc., Latham, New York) advanced through the lumen of the guiding catheter. Following the placement of the guidewire into the renal artery, the guiding catheter can be advanced across the diagnostic catheter close to the orifice of the renal artery and the diagnostic catheter is pulled out thereafter (Figures 5 A–D).

For renal artery revascularization via the brachial approach, various shapes of 6 Fr guiding catheters such as the “JR-4”, “AR-1” or “multipurpose” are available (Figures 1 and 4). Several low-profile renal stent devices (e.g., Palmaz Blue™, Cordis Corp.; Miami Lakes, Florida; RX Herculink Plus™, Guidant/Abbott Vascular, Temecula, California; Radix™, Sorin Biomedica Corp., Saluggia, Italy; Hippocampus™, Invatec Corp., Concesio Brescia, Italy) allow direct stenting in the vast majority of cases. As an alternative to a guiding catheter, a 90 cm 6 Fr sheath (e.g., Cook Inc., Bjaeverskov, Denmark) can be positioned near the origin of the renal artery. Selective cannulation of the renal artery has to be performed with a 4 Fr or 5 Fr diagnostic catheter of various shapes (“multipurpose” or others) to introduce a long 0.014 inch guidewire (300 cm) through the lesion into the renal artery. After removal of the 5 Fr diagnostic catheter, the stent can be placed. Angioplasty technique: Usually, an extra-support 0.014 inch guidewire with a soft tip (various manufacturers) is used. In cases of highly calcified tight lesions, predilatation should be performed starting with a 3 mm, followed by a 5 mm monorail balloon. If the 5 mm balloon does not expand completely, a cutting balloon (Boston Scientific Corp., Natick, Massachusetts) or a scoring balloon (Angiosculpt™, Biotronik, Bülach, Switzerland) should be used for plaque modulation. Otherwise, full stent expansion would be impossible. Pre-interventional pressure gradient measurement can provide helpful information about the hemodynamic relevance of RAS in uncertain cases, but is not recommended as a routine procedure; a reliable determination of the gradient would need a pressure wire, which is expensive and time-consuming. Moreover, every additional interventional step increases the risk of embolism. Whereas the measurement of resting pressure gradients was not predictive for the blood pressure response,23 Leesar et al reported a significant correlation of baseline hyperemic translesional pressure gradient with blood pressure response after successful revascularization.24 In 62 patients, a hyperemic systolic gradient (HSG) of > 21 mmHg measured with an 0.014-inch pressure wire following intrarenal injection of 30 mg of papaverine was the best predictor of improved blood pressure response after revascularization. Hypertension improvement at 1 year occurred in 84% of those with an HSG ≥ 21 mmHg compared to only 36% with an HSG 25 Hypertensive patients without RAS had a significantly lower RFC (20.1 ± 5.4) compared to hypertensive patients with RAS (RFC = 26.6 ± 9.1). Following stent revascularization, RFC decreased to 21.4 ± 6.7. Clinical responders (systolic blood pressure fell by ≥ 15 mmHg after revascularization) tended to have higher baseline RFCs than nonresponders and had a significantly greater reduction in RFC following stenting. Three-quarters of blood pressure responders had a baseline RFC ≥ 25; on the other hand, of those patients with a decrease in RFC > 4, 79% were responders to revascularization. RFC adds a functional assessment of the morphologic assessment of RAS. Analysis of RBG as a measure of microvascular renal flow may be helpful for evaluating the efficacy of embolic protection devices. For ostial lesions, balloon-expandable stents are standard. For post-ostial lesions, short self-expanding nitinol stents can be used alternatively (4 Fr shaft devices can be introduced via a 6 Fr guiding catheter!). The balloon- or stent-to-vessel ratio should be 1.1:1 for balloon-expandable stents, and in general, 1 mm oversized for self-expanding stents. Overexpansion of the stent compared to the vessel diameter should not exceed > 0.5 mm because of the potential risk of vessel perforation or dissection. For full stent expansion and wall coverage, dilatation time should be at least 20–30 seconds. Stent length should be kept as short as possible to cover the whole lesion, but not more. In particular, hypermobile kidneys stent fractures with consecutive acute thrombotic vessel occlusions have recently been reported.The role of drug-eluting stents (DES) and covered stents is still uncertain. The comparative but not randomized GREAT trial found a relative reduction of a 6-month restenosis rate of 50% (7% vs. 14%) in favor of the sirolimus-eluting stent; however, due to an underpowered study design, this difference was not statistically relevant.26 Excellent outcome results are reported for treating in-stent restenoses with either DES or covered >stents.27,28 A potential indication for DES such as the Taxus™ (Boston Scientific) might be small renal artery diameters (8,9,11 A new stent device dedicated to ostial stenting had recently been CE-marked: the ArchStent™ (Ostial Solutions, Mountainview, California, distributor: ev3, Inc., Bonn, Germany) (Figures 6 and 7). The Dual-balloon delivery system enables rapid, precise placement of the stent with the initially inflated locator balloon, which physically stops at the ostium and visually confirms the correct position. Inflating the second balloon results in stent placement, and further increasing the pressure in the locator balloon results in a flaring of the proximal stent end. The flared stent conforms anatomically to the aorto-ostial junction with increased proximal scaffolding and ostial coverage. Thus, the aorto-renal plaque is completely attached to the vessel wall, and recrossing the stent in cases of restenosis can easily be performed. The role of distal protection devices for renal interventions is still a matter of debate. So far, no dedicated protection device for renal application is available.29 The FiberNet® (Invatec) might be a safe and effective device for this indication; however, larger trials need still to confirm its potential benefits. A small randomized trial using the Angioguard™ device (Cordis) only resulted in better outcomes of distally protected renal angioplasty in terms of improved renal function when combining the filter with a glycoprotein IIb/IIIa receptor antagonist (Reopro).30 Post-interventional result documentation. After each intervention, selective and semiselective angiograms of the target lesion and the distal (intrarenal) arteries should be performed without a guidewire in place to document the final result and exclude peripheral embolism, dissection or perforation. Intravascular ultrasound is only indicated for study purposes. Treatment success is achieved if the residual diameter stenosis after angioplasty is Summary Even if recent randomized, controlled trials such as STAR31 and ASTRAL32, due to various reasons, did not show any clinical benefit of RAS stenting over medical treatment, there remain three accepted indications for renal stenting in selected patients. Both recent studies, in particular STAR, included a significant number of patients without severe stenoses resulting in inconclusive results of the overall underpowered study. In ASTRAL, the patient selection criterion was: “patients should be randomized if it is uncertain whether to revascularize.” The only conclusion of ASTRAL, thus, can be that patients with a weak clinical indication might not profit from revascularization. Unanswered is the outcome of patients with significant RAS with a certain indication for revascularization. The answer might be provided by the ongoing CORAL and RADAR trials.33,34 Proper patient selection and a safe interventional technique are the key elements of a clinically successful outcome of the patient following the procedure. In particular, patients with a short history of deterioration of renal function might reap the largest benefit from intervention. In patients with an advanced stage of renal failure, the indication for stenting of atherosclerotic RAS must be determined individually, considering the patient’s overall prognosis. In a recent prospective dual-center analysis of real-world registries, we could show a substantial improvement of renal function in patients with CKD stages 2 to 5 and a significant better survival in those patients.35

References

1. Plouin PF, Chatellier G, Darne B, Raynaud A. Blood pressure outcome of angioplasty in atherosclerotic renal artery stenosis: A randomized trial. The EMMA-study group. Hypertension 1998;31:823–829.

2. Trinquart L, Mounier-Vehier C, Sapoval M, et al. Efficacy of revascularization for renal artery stenosis caused by fibromuscular dysplasia. A systematic review and meta-analysis. Hypertension 2010;56:525–532.

3. Baert AL, Wilms G, Amery A, et al. Percutaneous transluminal renal angioplasty: Initial results and long-term follow-up in 202 patients. Cardiovasc Intervent Radiology 1990;13:22–28.

4. Bonelli FS, McKusick A,

5. Cluzel P, Raynaud A, Beyssen B, et al. Stenoses of renal branch arteries in fibromuscular dysplasia: Results of percutaneous transluminal angioplasty. Radiology 1994;193:227–232.

6. Dorros G, Prince C, Mathiak L. Stenting of renal artery stenosis achieves better relief of the obstructive lesion than balloon angioplasty. Cathet Cardiovasc Diagn 1993;29:191–198.

7. van de Ven PJ, Kaatee R, Beutler JJ, et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: A randomised trail. Lancet 1999;353:282–286.

8. Zeller T, Rastan A, Kliem M, et al. Impact of carbon coating on restenosis rate after stenting of atherosclerotic renal artery stenosis. J Endovasc Ther 2005;12:605–611.

9. Zeller T, Müller C, Frank U, et al. Gold coating and restenosis after primary stenting of ostial renal artery stenosis. Catheter Cardiovasc Interv 2003;60:1–6.

10. Sapoval M, Zähringer M, Pattynama P, et al. Low-profile stent system for treatment of atherosclerotic renal artery stenosis: The GREAT Trial. J Vasc Interv Radiol 2005;16:1195–1202.

11. Lederman RJ, Mendelsohn FO, Santos R, et al. Primary renal artery stenting: Characteristics and outcomes after 363 procedures. Am Heart J 2001;142:314–323.

12. Harding MB, Smith LR, Himmelstein SI, et al. Prevalence and associated risk factors in patients undergoing routine cardiac catheterization. J Am Soc Nephrol 1992;2:1608.

13. Missouris CG, Buckenham T, Cappuccio FP, MacGregor GA. Renal artery stenosis: A common and important problem in patients with peripheral vascular disease. Am J Med 1994;96:10–14.

14. Zierler RE, Bergelin RO, Davidson RC, et al. A prospective study of disease progression in patients with atherosclerotic renal artery stenosis. AJH 1996;9:1055–1061.

15. van Jaarsveld BC, Krijnen P, Pieterman H, et al. for the Dutch Renal Artery Stenosis Intervention Cooperative Study Group. The Effect of Balloon Angioplasty on hypertension in atherosclerotic renal-artery stenosis. N Engl J Med 2000;342:1007–1014.

16. Tollefson DFJ, Emst CB. Natural history of atherosclerotic renal artery stenosis associated with aortic disease. J Vasc Surg 1991;14:327–331.

17. Schreiber MJ, Pohl MA, Novick AC. The natural history of atherosclerotic and fibrous renal artery disease. Urol Clin North Am 1984;11:383–392.

18. Rimmer JM, Gennari FJ. Atherosclerotic renovascular disease and progressive renal failure. Ann Intern Med 1993;118:712–719.

19. Caps MT, Zierler RE, Polissar NL, et al. Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. Kidney Int 1998;53:735–742.

20. Safian RD, Textor SC. Renal-artery stenosis. N Engl J Med 2001;344:431–442.

21. Sang CN, Whelton PK, Hamper UM, et al. Etiologic factors of renovascular fibromuscular dysplasia: A case-controlled study. Hypertension 1989;14:472–479.

22. Feldman RL, Wargovich TJ, Bittl JA. No-touch technique for reducing aortic wall trauma during renal artery stenting. Catheter Cardiovasc Interv 1999;46:245–248.

23. Mitchell J, Subramanian R, White C, et al. Predicting blood pressure improvement in hypertensive patients after renal artery stent placement. Catheter Cardiovasc Interv 2007;69:685–689.

24. Leesar MA, Varma J, Shapira A, et al. Prediction of hypertension improvement after stenting of renal artery stenosis: Comparative accuracy of translesional pressure gradients, intravascular ultrasound, and angiography. J Am Coll Cardiol 2009;53:2363–2371.

25. Mahmud E, Smith TW, Palakodeti V, et al. Renal frame count and renal blush grade: Quantitative measures that predict the success of renal stenting in hypertensive patients with renal artery stenosis. JACC Cardiovasc Interv 2008;1:286–292.

26. Zähringer M, Sapoval M, Pattynama PM, et al. Sirolimus-eluting versus bare-metal low-profile stent for renal artery treatment (GREAT Trial): Angiographic follow-up after 6 months and clinical outcome up to 2 years. J Endovasc Ther 2007;14:460–468.

27. Zeller T, Rastan A, Schwarzwälder U, et al. Treatment of instent restenosis following stent-supported renal artery angioplasty. Catheter Cardiovasc Interv 2007;70:454–459.

28. Zeller T, Sixt S, Rastan A, et al. Treatment of reoccurring instent restenosis following reintervention after stent-supported renal artery angioplasty. Catheter Cardiovasc Interv 2007;70:296–300.

29. Henry M, Klonari s C, Henry I. Protected renal stenting with the PercuSurge GuardWire device: A pilot study. J Endovasc Ther 2001;8:227–237.

30. Cooper C, Haller S, Colyer WS, et al. Embolic protection and platelet inhibition during renal artery stenting. Circulation 2008;117:2752–2760.

31. Bax L, Woittiez AJ, Kouwenberg HJ, et al. Stent placement in patients with atherosclerotic renal artery stenosis and impaired renal function. Ann Intern Med 2009;150:840–848.

32. ASTRAL Investigators, Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009;361:1953–1962.

33. Cooper CJ. Stent revascularization for the prevention of cardiovascular and renal events among patients with renal artery stenosis and systolic hypertension: Rationale and design of the CORAL trial. Am Heart J 2006;152:59–66.

34. Schwarzwälder U, Hauk M, Zeller T. RADAR — A randomised, multi-centre, prospective study comparing best medical treatment versus best medical treatment plus renal artery stenting in patients with haemodynamically relevant atherosclerotic renal artery stenosis. Trials 2009;10:60 doi:10.1186/1745–6215–10–60.

35. Kalra PA, Chrysochou C, Green D, et al. The benefit of renal artery stenting in patients with atheromatous renovascular disease and advanced chronic kidney disease. Catheter Cardiovasc Interv 2010;75:1–10.

____________________________________________________________________

From the Heart Centre Bad Krozingen, Bad Krozingen, Germany. Disclosure: T. Zeller discloses receiving speakers bureau honoraria, a study grant and advisory board fees from Medtronic Invatec. No other relevant disclosures from the other authors. Address for correspondence: Prof. Dr. Thomas Zeller, Abteilung Angiologie, Herz-Zentrum, Bad Krozingen, Suedring 15, 79189 Bad Krozingen, Germany. E-mail: thomas.zeller@herzzentrum.de

Advertisement

Advertisement

Advertisement