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ML, Vascular Quality Initiative. Comparison of access type on perioperative outcomes after
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89. Oliveira-Pinto J, Oliveira N, Bastos-Gonçalves F, Hoeks S, Van Rijn MJ, Ten Raa S, Mansilha
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91. Ma WQ, Zhao Y, Wang Y, Han XQ, Zhu Y, Liu NF.Comparative efcacy of pharmacological interventions for contrast-induced nephropathy prevention after coronary angiography: a
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93. Kouvelos GN, Katsargyris A, Antoniou GA, Oikonomou K, Verhoeven EL.Outcome after
interruption or preservation of internal iliac artery ow during endovascular repair of abdominal aorto-iliac aneurysms. Eur J Vasc Endovasc Surg. 2016;52:621–34.
94. Bosanquet DC, Wilcox C, Whitehurst L, Cox A, Williams IM, Twine CP, British Society
of Endovascular Therapy (BSET). Systematic review and meta-analysis of the effect of
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95. Robalo C, Sousa J, Mansilha A.Internal iliac artery preservation strategies in the endovascular treatment of aortoiliac aneurysms. Int Angiol. 2018;37:346–55.
96. Oliveira-Pinto J, Martins P, Mansilha A. Endovascular treatment of iliac aneurysmal disease with internal iliac artery preservation: a review of two different approaches. Int Angiol.
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97. Daye D, Walker TG.Complications of endovascular aneurysm repair of the thoracic and
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98. Muhs BE, Jordan W, Ouriel K, Rajaee S, de Vries JP.Matched cohort comparison of endovascular abdominal aortic aneurysm repair with and without EndoAnchors. J Vasc Surg.
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99. Chaudhuri A, Kim HK, Valdivia AR.Improved midterm outcomes using standard devices
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100. Cannavale A, Lucatelli P, Corona M, Nardis P, Basilico F, De Rubeis G, Santoni M, Catalano
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5 Abdominal Aortic Aneurysm (AAA)

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101. D’Oria M, Mastrorilli D, Ziani B.Natural history, diagnosis, and management of type II endoleaks after endovascular aortic repair: review and update. Ann Vasc Surg. 2020;62:420–31.
102. Dijkstra ML, Zeebregts CJ, Verhagen HJM, Teijink JAW, Power AH, Bockler D, Peeters
P, Riambau V, Becquemin JP, Reijnen MMPJ, ENGAGE Investigators. Incidence, natural
course, and outcome of type II endoleaks in infrarenal endovascular aneurysm repair based
on the ENGAGE registry data. J Vasc Surg. 2020;71:780–9.
103. Yu HYH, Lindström D, Wanhainen A, Tegler G, Asciutto G, Mani K.An updated systematic
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104. Argyriou C, Georgiadis GS, Lazarides MK, Georgakarakos E, Antoniou GA. Endograft
infection after endovascular abdominal aortic aneurysm repair: a systematic review and metaanalysis. J Endovasc Ther. 2017;24:688–97.
105. Li HL, Chan YC, Cheng SW.Current evidence on management of aortic stent-graft infection:
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106. Shaw SE, Preece R, Stenson KM, De Bruin JL, Loftus IM, Holt PJE, Patterson BO.Short
stay EVAR is safe and cost effective. Eur J Vasc Endovasc Surg. 2019;57:368–73.
107. Montross BC, O’Brien-Irr MS, Koudoumas D, Khan SZ, Rivero M, Harris LM, Dosluoglu
HH, Cherr GS, Dryjski ML.The selection of patients for ambulatory endovascular aneurysm
repair of elective asymptomatic abdominal aortic aneurysm. J Vasc Surg. 2020;72:1347–53.
108. Mouton R, Rogers CA, Harris RA, Hinchliffe RJ.Local anaesthesia for endovascular repair
of ruptured abdominal aortic aneurysm. Br J Surg. 2019;106:74–81.
109. Faizer R, Weinhandl E, El Hag S, Le Jeune S, Apostolidou I, Shai SM, Lee CJ, Rosenberg
MS, Reed A, Fanola C.Decreased mortality with local versus general anesthesia in endovascular aneurysm repair for ruptured abdominal aortic aneurysm in the Vascular Quality
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110. Bennett KM, McAninch CM, Scarborough JE.Locoregional anesthesia is associated with
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112. Cheng TW, Maithel SK, Kabutey NK, Fujitani RM, Farber A, Levin SR, Patel VI, Jones DW,
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113. Moreno DH, Cacione DG, Baptista-Silva JC. Controlled hypotension versus normotensive resuscitation strategy for people with ruptured abdominal aortic aneurysm. Cochrane
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114. NICE Guideline Updates Team (UK). Permissive hypotension during transfer of people with
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IT, Papazoglou KO.The impact of aortic occlusion balloon on mortality after endovascular
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116. Ersryd S, Djavani-Gidlund K, Wanhainen A, Björck M.Editor’s choice—abdominal compartment syndrome after surgery for abdominal aortic aneurysm: a nationwide population
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118. Smidfelt K, Nordanstig J, Wingren U, Bergström G, Langenskiöld M.Routine open abdomen treatment compared with on-demand open abdomen or direct closure following open
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5 Abdominal Aortic Aneurysm (AAA)

Chapter 6
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Renal Artery Stenosis
6.1 Guidelines
6.1.1 American College ofCardiology Foundation/American
Heart Association
Renal artery disease guideline recommendations of the American Heart Association
[1] are:
Clinical Clues to the Diagnosis of Renal Artery Stenosis (Class I
recommendations)
1. The performance of diagnostic studies to identify clinically signicant renal
artery stenosis (RAS) is indicated in patients with the onset of hypertension
before the age of 30years. (Level of Evidence: B).
2. The performance of diagnostic studies to identify clinically signicant RAS is
indicated in patients with the onset of severe hypertension after the age of
55years. (Level of Evidence: B).
3. The performance of diagnostic studies to identify clinically signicant RAS is
indicated in patients with the following characteristics: (a) accelerated hypertension (sudden and persistent worsening of previously controlled hypertension);
(b) resistant hypertension (dened as the failure to achieve goal blood pressure
in patients who are adhering to full doses of an appropriate 3-drug regimen that
includes a diuretic); or (c) malignant hypertension (hypertension with coexistent
evidence of acute end-organ damage, ie, acute renal failure, acutely decompensated congestive heart failure, new visual or neurological disturbance, and/or
advanced [grade III to IV] retinopathy). (Level of Evidence: C).
4. The performance of diagnostic studies to identify clinically signicant RAS is
indicated in patients with new azotemia or worsening renal function after the
administration of an ACE inhibitor or an angiotensin receptor blocking agent.
(Level of Evidence: B).
Switzerland AG 2023
E. S. Debus, R. T. Grundmann, Evidence-based Therapy in Vascular Surgery,
https://doi.org/10.1007/978-3-031-47397-5_6
161© The Author(s), under exclusive license to Springer Nature

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6 Renal Artery Stenosis
5. The performance of diagnostic studies to identify clinically signicant RAS is
indicated in patients with an unexplained atrophic kidney or a discrepancy in
size between the 2 kidneys of greater than 1.5cm. (Level of Evidence: B).
6. The performance of diagnostic studies to identify clinically signicant RAS is
indicated in patients with sudden, unexplained pulmonary edema (especially in
azotemic patients). (Level of Evidence: B).
Diagnostic Methods (Class I recommendations)
1. Duplex ultrasonography is recommended as a screening test to establish the
diagnosis of RAS. (Level of Evidence: B).
2. CTA (in individuals with normal renal function) is recommended as a screening
test to establish the diagnosis of RAS. (Level of Evidence: B).
3. MRA is recommended as a screening test to establish the diagnosis of RAS. (Level
of Evidence: B).
Indications for Revascularization (Class IIb recommendations)
Asymptomatic stenosis
1. Percutaneous revascularization may be considered for treatment of an asymp-
tomatic bilateral or solitary viable kidney with a hemodynamically signicant
RAS. (Level of Evidence: C).
2. The usefulness of percutaneous revascularization of an asymptomatic unilateral
hemodynamically signicant RAS in a viable kidney is not well established and
is presently clinically unproven. (Level of Evidence: C).
Hypertension (Class IIa recommendation)
1. Percutaneous revascularization is reasonable for patients with hemodynamically
signicant RAS and accelerated hypertension, resistant hypertension, malignant
hypertension, hypertension with an unexplained unilateral small kidney, and
hypertension with intolerance to medication. (Level of Evidence: B).
Preservation of Renal Function
1. Percutaneous revascularization is reasonable for patients with RAS and progres-
sive chronic kidney disease with bilateral RAS or a RAS to a solitary functioning
kidney. (Class IIa/Level of Evidence: B).
2. Percutaneous revascularization may be considered for patients with RAS and
chronic renal insufciency with unilateral RAS. (Class IIb/Level of Evidence: C).
Impact of RAS on Congestive Heart Failure and Unstable Angina
1. Percutaneous revascularization is indicated for patients with hemodynamically
signicant RAS and recurrent, unexplained congestive heart failure or sudden,
unexplained pulmonary edema. (Class I/Level of Evidence: B).
2. Percutaneous revascularization is reasonable for patients with hemodynamically
signicant RAS and unstable angina. (Class IIa/Level of Evidence: B).
Endovascular treatment for RAS (Class I recommendations)

6.1 Guidelines
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1. Renal stent placement is indicated for ostial atherosclerotic RAS lesions that
meet the clinical criteria for intervention. (Level of Evidence: B).
2. Balloon angioplasty with bailout stent placement if necessary is recommended
for bromuscular dysplasia lesions. (Level of Evidence: B).
Surgery for RAS (Class I recommendations)
1. Vascular surgical reconstruction is indicated for patients with bromuscular dys-
plastic RAS with clinical indications for interventions (same as for percutaneous
transluminal angioplasty), especially those exhibiting complex disease that
extends into the segmental arteries and those having macroaneurysms. (Level of
Evidence: B).
2. Vascular surgical reconstruction is indicated for patients with atherosclerotic
RAS and clinical indications for intervention, especially those with multiple
small renal arteries or early primary branching of the main renal artery. (Level of
Evidence: B).
3. Vascular surgical reconstruction is indicated for patients with atherosclerotic
RAS in combination with pararenal aortic reconstructions (in treatment of aortic
aneurysms or severe aortoiliac occlusive disease). (Level of Evidence: C).
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6.1.2 European Society ofCardiology (ESC) andEuropean
Society forVascular Surgery (ESVS)
The ESC and ESVS guidelines [2] consider renal artery disease (RAD) when renal
artery stenosis (RAS) is ≥60%, although additional functional assessment by haemodynamic criteria is advisable.
6.1.2.1 Clinical Situations Raising Suspicion forRenal Artery Disease
• Onset of hypertension before the age of 30years.
• Onset of severe hypertension after the age of 55years, when associated with
chronic kidney disease or heart failure.
• Hypertension and abdominal bruit.
• Rapid and persistent worsening of previously controlled hypertension.
• Resistant hypertension (i.e. other secondary form unlikely and target not achieved
despite four drug classes including a diuretic and mineralocorticoid-receptor
antagonist in appropriate doses).
• Hypertensive crisis (i.e. acute renal failure, acute heart failure, hypertensive
encephalopathy, or grade 3 to 4 retinopathy).
• New azotemia or worsening of renal function after treatment with renin-
angiotensin- aldosterone system (RAAS) blockers.

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6 Renal Artery Stenosis
• Unexplained atrophic kidney or discrepancy in kidney size, or unexplained renal
failure.
• Flash pulmonary oedema.
6.1.2.2 Diagnostic Strategies
• Duplex ultrasound (as rst-line), CTA and MRA are recommended imaging
modalities to establish a diagnosis of RAD. (Class I recommendation/Evidence
level B).
• DSA may be considered to conrm a diagnosis of RAD when clinical suspicion
is high and the results of non-invasive examinations are inconclusive. (Class IIb
recommendation/Level of evidence C).
• Renal scintigraphy, plasma renin measurements before and after angiotensin-
converting enzyme inhibitor (ACEI) provocation and vein renin measurements
are not recommended for screening of atherosclerotic RAD. (Class III recommendation/Evidence level C).
6.1.2.3 Recommendations forTreatment Strategies forRenal
Artery Disease
Medical therapy
• ACEIs/ARBs (angiotensin receptor blockers) are recommended for treatment of
hypertension associated with unilateral RAS. (Class I recommendation/Evidence
level B).
• Calcium channel blockers, beta-blockers and diuretics are recommended for
treatment of hypertension associated with renal artery disease. (Class I recommendation/Level of evidence C).
• ACEIs/ARBs may be considered in bilateral severe RAS and in the case of ste-
nosis in a single functioning kidney, if well-tolerated and under close monitoring. (Class IIb recommendation/Level of evidence B).
Revascularisation
• Routine revascularisation is not recommended in RAS secondary to atheroscle-
rosis. (Class III recommendation/Level of evidence A).
• In cases of hypertension and/or signs of renal impairment related to renal arterial
bromuscular dysplasia, balloon angioplasty with bailout stenting should be
considered. (Class IIa recommendation/Level of evidence B).
• Balloon angioplasty, with or without stenting, may be considered in selected
patients with RAS and unexplained recurrent congestive heart failure or sudden
pulmonary oedema. (Class IIb recommendation/Level of evidence C).
• In the case of an indication for revascularisation, surgical revascularisation
should be considered for patients with complex anatomy of the renal arteries,

6.1 Guidelines
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after a failed endovascular procedure or during open aortic surgery. (Class IIa
recommendation/Level of evidence B).
165
6.1.3 Society forCardiovascular Angiography
andInterventions (SCAI)
6.1.3.1 Clinical Scenarios inWhich Treatment ofSignicant RAS May
BeConsidered [3]
Appropriate care:
• Cardiac disturbance syndromes (ash pulmonary oedema or acute coronary syn-
drome with severe hypertension).
• Resistant hypertension (uncontrolled hypertension with failure of maximally tol-
erated doses of at least 3 antihypertensive agents, one of which is a diuretic, or
intolerance to medications).
• Ischaemic nephropathy with chronic kidney disease (CKD) with estimated
GFR<45ml/min and global renal ischaemia (unilateral signicant RAS with a
solitary kidney or bilateral signicant RAS) without other explanation.
May be appropriate care:
• Unilateral RAS with CKD (eGFR <45ml/min).
• Unilateral RAS with prior episodes of congestive heart failure (stage C).
• Anatomically challenging or high-risk lesions (early bifurcation, small vessel,
severe concentric calcication, and severe aortic atheroma or mural thrombus).
Rarely appropriate care:
• Unilateral, solitary or bilateral RAS with controlled blood pressure and normal
renal function.
• Unilateral, solitary or bilateral RAS with kidney size <7cm in pole-to-pole length.
• Unilateral, solitary or bilateral RAS with chronic end-stage renal disease on
hemodialysis >3months.
• Unilateral, solitary or bilateral renal artery chronic total occlusion.
(Note: signicant RAS is an angiographically moderate lesion (50–70%) with physiologic conrmation of severity or a>70% stenosis).
6.1.4 Fibromuscular Dysplasia- Statement fromtheAHA
A scientic statement from the American Heart Association [4] species the following indications for renal arterial revascularization in patients with renal artery bromuscular dysplasia (FMD):

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1. Resistant hypertension (failure to reach goal blood pressures in patients on an
appropriate 3-drug regimen including a diuretic).
2. Hypertension of short duration with the goal of a cure of hypertension.
3. Renal artery dissection; rarely is intervention needed, but if so, stenting is gener-
ally the procedure of choice.
4. Renal artery aneurysm(s); surgical resection, endovascular coiling, or placement
of a covered stent is usually used.
5. Branch renal artery disease and hypertension; some lesions can be treated with
PTA, but if this is not possible, surgical revascularization may be required, often
with bench repair.
6. Preservation of renal function in the patient with severe stenosis, especially in
the pediatric population with perimedial broplasia or intimal broplasia.
Randomized, controlled trials of revascularization versus medical therapy in patients
with renal artery FMD have not been performed. The negative trials on stent implantation for atherosclerotic renal artery disease do not apply to patients with FMD
given the differing pathophysiology and natural history of these 2 vascular disorders. The natural history of medial broplasia is generally benign.
PTA of the renal artery is the procedure of choice for patients with renal artery
FMD and hypertension in the appropriate clinical setting. The typical FMD patient
with multifocal disease of the main renal artery is rst offered PTA. There are
patients, however, in whom the expected outcome from surgery may be better than
that expected with PTA. Examples include patients with small renal arteries
(<4mm), branch disease, especially when associated with aneurysms, or extensive
intimal or perimedial broplasia. Secondary surgical repair after failed PTA should
be considered early in the decision process before chronic ischemia leads to loss of
cortical thickness.
6 Renal Artery Stenosis
6.2 Results
6.2.1 Endovascular Intervention
6.2.1.1 Systematic Reviews/Meta-Analyses
A Cochrane Review compared the effectiveness of balloon angioplasty (with and
without stenting) with medical therapy for the treatment of atherosclerotic renal
artery stenosis in patients with hypertension [5]. Eight randomised controlled trials
(RCTs) comparing balloon angioplasty with medical therapy in 2222 hypertensive
patients with haemodynamically signicant renal artery stenosis (greater than 50%
reduction in luminal diameter) and with a minimum follow-up of 6 months were
included. The available data were insufcient to conclude that revascularisation in
the form of balloon angioplasty, with or without stenting, is superior to medical
therapy for the treatment of atherosclerotic renal artery stenosis in patients with
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