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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3657_Библиотеки_им_академика_М_И_Перельмана.pdf
294
A. Uacker and A. H. Matsumoto
Fig. 26.1 (a) A large aortic plaque is shown engulng and extending
into the origin of the left main renal artery causing an ostial ARAS
(arrow). (b) A contrast-enhanced coronal MIP image from a MRA
shows an irregular stenosis (arrow) of the proximal left main renal
Key Point
Renal artery stenosis accounts for <2% of patients
with hypertension.
The causes for RAS of the main, segmental, or lobar renal
arteries can be divided into three major categories: (1) atherosclerotic RAS (ARAS), (2) bromuscular dysplasia (FMD),
and (3) other. More than 90% of RAS cases are due to atherosclerosis [4], with the majority of the remaining patients having FMD as the etiology. ARAS is seen mainly in older
patients (> 60years old) with a family history of diffuse atherosclerotic cardiovascular disease (CV) and/or a history of
smoking, diabetes, hypertension, dyslipidemia, and/or obesity. Pathologically, the stenosis is caused by a buildup of atherosclerotic plaque that often originates in the aorta and
extends into and engulfs the ostium (origin) of the renal artery
(Fig.26.1). ARAS is usually eccentric and asymmetric and
can be calcied. On occasion, ARAS can be isolated to the
main trunk (midportion) of the renal artery (Fig. 26.2).
Although ARAS involving the non-ostial portion of a main
renal artery can occur, ostial ARAS is much more common.
Signicant ARAS is bilateral in ~20% of patients [7].
ARAS should be considered to be a systemic vascular disorder that is characterized by the activation of multiple inammatory and immune pathways and associated with signicant
CV morbidity and mortality [5]. It should also be considered
artery consistent with an ARAS, with a mild stenosis of the proximal
right renal artery noted. Note the luminal irregularity of the aorta demonstrating the diffuse nature of atherosclerotic disease
Fig. 26.2 An atherosclerotic plaque is shown involving the main trunk
of the left main renal artery causing an ARAS (arrow)
a progressive disorder, but the ability to predict which
patients will progress or remain stable is not well dened [8].
However, optimum medical management of the CV risk factors appears to have a positive impact on progression of disease and reducing the morbidity and mortality [2, 3, 7].
Fibromuscular dysplasia (FMD) is a non-atherosclerotic,
noninammatory disease of medium-sized arteries which
may result in an arterial stenosis, dissection, and/or aneurysm. Although the most common site of FMD involvement
is the renal arteries, the prevalence of FMD in the general
26 Renal Artery Stenosis
295
population and involvement of the carotid and vertebral
arteries are much more common than once believed. FMD
has also been seen in the brachial, mesenteric, coronary, and
iliac arteries. FMD tends to manifest in younger patients
(less than 60 years old) with a female predominance (10
females:1 male). Patients with FMD have fewer CV risk factors than patients with ARAS.FMD has a familial component with cases seen in multiple generations of the same
family, but no etiologic genes have been identied to date,
and the familial manifestation may be affected by many epigenetic factors. FMD may also have some overlap with other
vascular connective tissue diseases, such as Loeys-Dietz and
Ehlers-Danlos syndromes [8].
Key Point
Fibromuscular dysplasia involves the medium-sized
arteries and can result in stenosis, dissection, or aneurysm. Arteries most commonly involved:
• Renal (most common)
• Carotid
• Iliac
• Vertebral
• Mesenteric
• Coronary
• Brachial
FMD tends to involve the mid- to distal portions of the
main renal arteries and/or its segmental branches, is bilateral
in >33% of patients, and often involves more than one
vascular territory [9–11]. In addition, the intrarenal inammatory processes and sequela seen in ARAS are less of an
issue with RAS caused by FMD [5]. Signicant impairment
of renal function due to FMD is very rare as compared to
ARAS. For nomenclature purposes, FMD is classied as
either being unifocal (involving ≤1cmof the artery) or multifocal (involving >1cm of the artery) (Figs.26.3 and 26.4).
The unifocal type of FMD tends to appear as a concentric
area of narrowing or band-like stenosis and is most often
seen in children and very young patients. Pathologically, one
or more of the layers of the arterial wall are abnormal, with
areas of intimal, medial, or adventitial dysplasiaor hyperplasia, or absence of the media with or without areas of segmental arterial dilation. The stenosis is not due to atherosclerotic
material but rather, results from excessive intimal or brous
material.
The diagnosis of FMD is most often made on an imaging
study in which the artery appears with pleat-like narrowings,
alternating with areas of vessel dilation, giving it an appearance often described as a “string of pearls” or “beads on a
string.” FMD can involve a long arterial segment (>3cm) or
be very focal (<1cm) or have a combination of both appearances. FMD can involve the main renal artery, its branches,
or both locations (see Figs.26.3 and 26.4).
Other causes for RAS can be seen in Table26.1. In composite, these other etiologies comprise less than 5% of
Fig. 26.3 (a) Unifocal (<1cm in length) FMD is shown involving the left main renal artery just distal to an early lower pole renal artery branch.
(b) A coronal MIP image from a contrast-enhanced MRA showsunifocal changes of FMD in the distal right main renal artery (arrow)
296
Fig. 26.4 (a) Multifocal
(>1cm in length) FMD is
displayed involving the left
main renal artery trunk (larger
arrow), extending into both
segmental renal artery
branches (smaller arrows). (b)
Volume-rendered
reconstructed 3D image
shows the endograft in the
abdominal aorta and the FMD
changes involving the left
main (arrow) and segmental
renal arteries. (c, d)
Maximum intensity projection
(MIP) images from a CTA in
a patient with an aortic
endograft show multifocal
FMD of the distal left main (c
= coronal MIP,arrow) and the
upper segmental branch (d =
axial MIP, arrow) renal
arteries
A. Uacker and A. H. Matsumoto
Table 26.1 Other causes for RAS of the large- to medium-size renal
arteries
Causes of renal artery stenosis
Atherosclerosis Trauma
Fibromuscular dysplasia Extrinsic compression (median arcuate
Vasculitis (i.e.,
Takayasu)
Neurobromatosis Segmental arterial mediolysis
Radiation-induced
arteritis
ligament)
Aortic or spontaneous renal artery
dissection
Arterial thromboembolism
patients with RAS.The pathophysiological changes that are
associated with each of these disease entities affect the
patient demographics, disease epidemiology, natural history,
imaging appearance, and treatment decisions and options for
this diverse group of patients.
Clinical Indications
The clinical presentation, evaluation, physical exam, and
imaging ndings will vary depending upon the cause of
RAS. Therefore, the evaluation of each patient should
involve a tailored approach specic to the demographics of
each patient. Patients with FMD tend to have a high preva-
lence of migraine headaches and pulsatile tinnitus [9, 10]. In
addition, patients with FMD have a higher incidence of intracranial and visceral aneurysms and are more likely to develop
spontaneous coronary and visceral artery dissections as compared to the general population [9, 10]. Therefore, the cur-
rent recommendation is that patients with FMD undergo a
computed tomographic angiography (CTA) screening of the
head and neck, visceral and iliac arteries to evaluate for the
presence of aneurysms, dissections or signicant obstructive
FMD lesions.
ARAS tends to occur in older patients with multiple CV
risk factors. These patients often have diffuse atherosclerotic
disease involving their peripheral, coronary, mesenteric, and/
or cerebral vascular beds. Therefore, in addition to sudden
worsening of or much more labile hypertension, patients
with ARAS may have associated symptoms and ndings
related to diffuse CV disease such as transient ischemic
attacks (TIAs), stroke, cardiac angina, myocardial infarction,
recurrent bouts of heart failure, shortness of breath, intestinal
angina, claudication, aortic aneurysm, and/or renal impairment. Features that suggest that the hypertension, renal
insufciency, and/or sudden episodes of heart failure may be
related to signicant ARAS are seen in Table26.2.
A good history should be obtained to assess for comor-
bidities and other symptoms related to the diffuse CV dis-
26 Renal Artery Stenosis
297
Table 26.2 Clinical clues to suggest that a physiologically signicant
ARAS may be present
Presence of diffuse atherosclerotic cardiovascular disease and
associated risk factors
Sudden onset or signicant worsening of hypertension in a patient
>55years old
Episodes of unexplained pulmonary edema, especially with normal
resting LV function
Unexplained atrophic kidney or size discrepancy >1.5cm between
the kidneys
Development of new or worsening renal function with the initiation
of an ACE inhibitor or ARB agent (although microvascular disease is
most often the reason for this observation)
Sudden worsening in either normal renal function or stable chronic
renal insufciency
a
Adapted from Ref. [4]
a
ease or involvement of other vascular beds. A physical
examination should include a detailed peripheral pulse evaluation assessing for decits in and symmetry of perfusion to
the extremities, as well as looking for any evidence for spontaneous cholesterol embolization or the presence of tissue
loss due to poor perfusion to the extremities. Auscultation for
carotid, renal, abdominal, or pelvic bruits will help to detect
if there is involvement of multiple vascular beds.
Laboratory evaluation should, at minimum, include a
serum creatinine and BUN level to assess renal function; a
urinalysis to screen for an occult infection, red blood cells, or
casts (to assess for glomerulonephritis); and a urine creatinine to albumin ratio to assess for proteinuria and underlying
renal parenchymal disease. A 24-h urine protein to further
assess for the severity of proteinuria may be indicated in
some patients. Patients with a urine albumin to creatinine
ratio≤22.5mg/g respond better to renal stent therapy than
patients with ratios >22.5mg/g or signicant proteinuria [12,
13]. Imaging evaluation usually begins with a renal duplex
ultrasound (US) with Doppler to assess peak systolic velocities (>220cm/s is abnormal), aortic to renal ratios (>3.5 is
abnormal), and pulsus tardus (suggests presence of a stenosis). A renal parenchymal resistive index >0.8 suggests signicant underlying intrarenal parenchymal disease. Although
a duplex US exam is relatively inexpensive, avoids use of
radiation, and is readily available, obtaining a good study is
very dependent on the skills of the technologist and body
habitus of the patient: large body mass index patients are
hard to image with US.A duplex study does not consistently
dene the number of renal arteries, the anatomy of the distal
main renal artery or its proximal branches [4, 14].
Key Point
A patient with RAS and anurine albumin to creatinine
ratio ≤ 22.5 mg/g responds better to stenting than
patientswith a ratio >22.5mg/g or signicant proteinuria.
Key Point
Renal artery duplex ultrasound indications of RAS:
• Peak systolic velocity>220cm/s
• Aortic to renal ratio>3.5
• Pulsus tardus (tardus parvus)
CTA is the best noninvasive imaging study for spatial resolution and dening the renal arterial anatomy and number of
renal arteries. It is technology dependent: the better the CT
scanner, the better the images. It does require the use of radiation and iodinated contrast material. CTA is relatively contraindicated in patients with a signicant allergy to iodinated
contrast material or severe, non-dialysis-dependent renal
insufciency [4, 14]. Iodinated contrast has been attributed to
causing acute kidney injury, especially in patients with underlying chronic kidney disease and/or dehydration [15].
The best magnetic resonance angiography (MRA) images
of the renal arteries are obtained using state-of-the art 1.5
or 3T MRI units and the administration of an intravenous
gadolinium- based contrast agent. MRA does not involve use
of any ionizing radiation. Patients with allergies to iodinated
contrast or renal insufciency with an eGFR ≥30 can have
an MRA.However, patients must be able to hold their breath,
remain still for longer periods of image acquisition (as compared to CTA), and not be claustrophobic. Obtaining a good
MRA study is more technologist dependent than CTA,
but much less so than a renal duplex US [4, 14]. Patients
who are on dialysis or have a GFR <30 should not receive
gadolinium- based contrast agents due to the risk of developing a potentially lethal condition called nephrogenic systemic brosis [16].
Catheter-based digital subtraction angiography (DSA)
remains the gold standard for determining the number of
renal arteries and evaluating for the presence of a hemodynamically signicant RAS. DSA subtracts the background
bony landmarks and bowel gas and therefore only shows
the contrast outlining the lumen of the vessels in which contrast is injected. Unsubtracted digital images, which leave
the background bony and bowel gas information can also be
created. Catheter-based DSA is invasive and requires the use
of iodinated contrast and ionizing radiation. DSA images
are only two-dimensional and may over- or underestimate
the degree of arterial stenosis. Therefore, determining the
hemodynamic signicance of a RAS in a patient with suspicion for RVH should be a standard part of the catheter-based
evaluation (Fig. 26.5). Patients with RAS who are found
to have a mean translesional pressure gradient ≥10% or a
hyperemia- induced systolic gradient ≥21 mmHg are more
likely to benet from renal artery angioplasty and/or stent
therapy [4, 17–19].
298
Fig. 26.5 When a
translesional pressure gradient
is measured, a 0.014 inch
pressure wire is advanced
distal to the RAS and a
pressure tracing is obtained
(Pd), while a simultaneous
pressure is measured via a
guiding catheter positioned in
the aorta proximal to the RAS
(Pa). The pressure tracings are
superimposed and a
peak-to-peak systolic pressure
gradient can be easily
visualized. The mean pressure
gradient can also be
calculated by the machine,
accounting for both the
systolic and diastolic
components of the arterial
pressure gradient
A. Uacker and A. H. Matsumoto
Fig. 26.6 Image (a) is from an IVUS catheter positioned at the origin
of the right main renal artery. The image shows the IVUS catheter as a
black spot surrounded by a white halo. The yellow outline denes the
lumen of the renal artery, with the orange line representing the artery
wall. The distance between the arterial lumen and arterial wall repre-
Key Point
Angiography ndings indicating a patient is more
likely to benet from angioplasty or stenting:
• Mean translesional pressure gradient ≥10%
• Hyperemia-induced systolic gradient ≥21mmHg
sents the plaque material causing the asymmetric ARAS.Image (b) is a
virtual histology image created by the IVUS machine software, with the
yellow color representing cholesterol-based plaque and the green color
representing more brous-like material
Intravascular ultrasound (IVUS) employs a catheter with
an ultrasound transducer embedded in its tip. The IVUS
catheter is placed within the renal artery and provides images
of the arterial anatomy from this intraluminal location. In
addition to visualizing the anatomy, the effect of the RAS on
fractional ow reserve and the virtual histologic nature of the
RAS can be determined by the software program in the IVUS
machine (Fig. 26.6). Therefore, IVUS may be used to
26 Renal Artery Stenosis
299
supplement traditional catheter-based DSA to better dene
the RAS and assess the anatomic result of an intervention
[19, 20]. However, use of an IVUS catheter requires the
manipulation of an additional device within the arterial system, which increases the costs, length of the procedure, and
risks of a complication.
Conventional Therapy
Managing the diffuse atherosclerotic disease and its associated CV risk factors is paramount to achieving good outcomes in patients with ARAS [4]. Therefore, optimizing
medical therapies for hypertension, dyslipidemia, diabetes,
and chronic renal insufciency, as well as appropriate use of
antiplatelet agents and beta-blockers, is particularly important for patients with ARAS.For patients with renal artery
FMD, determining if there is also involvement of the cerebral and mesenteric vascular beds is important for the longitudinal management and treatment planning of these patients.
If an associated renal artery aneurysm is also present,
thoughtful planning and staging of or combining interventions will be necessary [9, 10]. Any associated renal, mesenteric, or intracranial aneurysms or obstructive lesions of the
mesenteric, carotid, vertebral, or iliac arteries should also be
treated (see Chaps. 25 and 46 for more information on management of visceral and cerebral aneurysms, respectively).
Interventional Therapy
If there is clinical suspicion of a physiologically signicant
ARAS (Table 26.2) and a noninvasive imaging study suggests the presence of a hemodynamically signicant RAS,
catheter-based angiography and an endovascular intervention should be undertaken. However, the ndings of the
CORAL trial and other randomized controlled studies on
renal artery stent placement for patients with ARAS have
shown that patients on optimum medical therapy with signicant proteinuria [12, 13] and/or a non-hemodynamically
Key Point
The CORAL trial and other RCTs have shown that
patients with signicant proteinuria and/or a nonhemodynamically signicant RAS should not undergo
a stent procedure; instead, they should be managed
with aggressive medical therapy.
Renal artery stenting is indicated inpatients with clinical sequela related to a RAS and a hemodynamically
signicant translesional pressure gradient and a urine
albumin to creatinine ratio less than or equal to 22.5.
signicant RAS [4, 17–19] are not likely to benet from
renal stent therapy. Therefore, patients with RAS and signicant proteinuria and/or a non-hemodynamically signicant
RAS should not undergo a stent procedure, but rather be
managed with aggressive medical therapy [4, 5, 7, 12, 13].
Once a patient without signicant proteinuria or signicant medical renal disease has been determined to have an
ARAS, a catheter-based angiogram should be performed to
better dene the lesion, and a translesional pressure gradient
should be measured (see Fig.26.5). If the translesional pressure gradient is hemodynamically signicant, renal artery
stent therapy should be performed (Fig.26.7). Treatment of
a total renal artery occlusion ipsilateral to a kidney that measures >8cm in length may also be benecial (Fig.26.8) [4,
8]. A procedural success rate of >95% and a major complica-
tion rate of <2% should be expected. Patients with recent
worsening in renal function, more difcult to control hypertension, and episodes of sudden onset of congestive heart
failure (ash pulmonary edema) are most likely to benet
from the endovascular procedure. Improvement or stabilization of renal function, better blood pressure control on fewer
or the same number of medications, and fewer episodes of
ash pulmonary edema can be expected in a high percentage
of these patients [4, 5, 7, 8, 13, 21]. Otherwise, treatment of
a hemodynamically signicant stenosis is unlikely to cure
hypertension in patients with ARAS.In-stent restenosis can
be expected in about 20% of patients within 3years. Balloon
angioplasty of ARAS is associated with poorer technical outcomes and higher recurrence rates than with stent placement
and is therefore not recommended for the treatment of
ARAS.Use of drug-eluting stents and drug-coated balloon
angioplasty for ARAS has not been sufciently evaluated.
For patients with signicant RAS due to FMD, percutaneous transluminal renal angioplasty (PTRA) alone has been
shown to be effective for most patients and is associated with
a >95% procedural technical success rate, major complication rate <2%, and a freedom from restenosis of >80%
(Fig.26.9) [10, 11, 22–24]. Repeat PTRA can be performed
for recurrences with good results. Unlike ARAS, hypertension due to FMD can be cured in up to 40% of patients, especially in younger patients with a shorter duration of
hypertension and no evidence for intrinsic renal parenchymal disease (Fig.26.10) [22–24]. Procedure-related dissection or rupture after balloon angioplasty may require
placement of a covered or bare metal stent to obviate open
surgical repair.
Key Point
Patients with RAS due to FMD should be treated with
balloon angioplasty only.
300
A. Uacker and A. H. Matsumoto
Fig. 26.7 (a) A digital subtraction angiography (DSA) shows the
asymmetric narrowing (arrow) of the ostium (origin) of the left main
renal artery consistent with an ARAS. (b) A spot image shows the undeployed stent (larger arrow) mounted between the two radio-opaque
markers (two smaller arrows)of an angioplasty balloon catheter. The
stent is being positioned across the ARAS at the left renal artery ostium.
(c) A spot image shows the inated angioplasty balloon expanding the
stent (dened by the two arrows). (d) An unsubtracted digital image
with contrast injected shows the nicely positioned, fully expanded stent
and the widely patent ostium (arrow) of the left renal artery
26 Renal Artery Stenosis
301
Fig. 26.8 (a) DSAimage shows occlusion of the bilateral main renal
arteries in a patient with sudden worsening of chronic renal insufciency who is now requiring dialysis therapy. The occlusion of the left
main renal artery (small arrow) was felt to be due to progression of
Fig. 26.9 (a) DSA shows single main renal arteries bilaterally, with
pleat-like irregularities of the distal right main renal artery consistent
with multifocal FMD (arrow). (b) Selective DSA imageof the right
main renal artery with a guidewire in place again shows the multifocal
FMD (arrow). A signicant pressure gradient across the area of FMD
was present. (c) Spot image with the angioplasty balloon inated in the
ARAS. (b) Catheter-based DSA image after placing a stent across the
left renal artery occlusion shows a widely patent left main renal artery
(arrow). The patient was able to come off dialysis and the renal function
stabilized with a serum creatinine of 3.2mg/dl
distal right main renal artery is seen (arrow). (d) Catheter-based DSA
image after balloon angioplasty reveals a markedly improved caliber of
the artery and less irregularity of the distal right main renal artery
(arrow). The systolic pressure gradient was reduced to less than
5mmHg
302
Fig. 26.9 (continued)
A. Uacker and A. H. Matsumoto
Fig. 26.10 The graph shows the marked improvement in the mean sys-
tolic and diastolic blood pressures of a cohort of 66 patients with renal
artery FMD before (topline, pre-PTRA) and after (bottom line, post-PTRA)
PTRA, with a mean follow-up (F-U) period of 39months. After PTRA,
41% (27/66) of the patients were cured (off all blood pressure medications).
The inset angiographic images are from one patient beforePTRA, immediately after (post-PTRA), and 12 months after the PTRA procedure (12month F-U). The 12-month follow-up angiogram shows the interval
vascular remodeling of the right renal artery that has occurred (Reprinted
with permission from the RSNAfrom Tegtmeyer etal. [22])
26 Renal Artery Stenosis
The How To
1. The common femoral or radial artery is accessed
with or without ultrasound guidance, and a vascular
sheath is inserted using the Seldinger technique.
2. A guidewire is advanced into the abdominal aorta
followed by placement of a multisidehole catheter
at the level of the renal arteries over the guidewire.
3. Contrast is injected via the catheter, and a DSA of
the abdominal aorta is performed to verify the number and size of the renal arteries and the location
26.7a and 26.9a).
4.
the affected renal artery is carefully selected.
5. A pressure wire is advanced across the RAS, and a
translesional pressure gradient is measured (see
26.5).
6. Once the RAS is determined to be hemodynami-
26.7b–d), and RAS due to
26.9b–d).
(a) When performing PTRA or stent placement,
303
inset images of the renal artery FMD after angioplasty) and
“heal” in a dilated state. Patients are usually maintained on a
baby aspirin and sometimes another antiplatelet agent such
as clopidogrel.
After the endovascular intervention, patients are seen in
follow-up as an outpatient at 6weeks, 6months, 12months,
and yearly thereafter. At each clinic visit, a renal artery
duplex exam is obtained to assess for arterial patency and
restenosis. The ndings on the duplex study are correlated
with the patient’s clinical symptoms, blood pressure, renal
function, and medications. For patients with ARAS, assessment for progression of the underlying CV disease should
also be evaluated by targeted history queries (i.e., TIAs,
intestinal or cardiac angina, and arm or leg claudication) and
physical examination (pulse and extremity evaluation and
auscultating for bruits). For patients with RAS due to FMD,
in addition to managing blood pressure concerns, if the
patient has FMD involving other vascular beds, attention
should be directed toward appropriate clinical and imaging
follow-up.
Conclusion
stent or dilate the renal artery is based on the
diameter of the adjacent normal renal artery
segment. The stent is chosen to cover the entire
entire segment of FMD should be balloon
dilated. The patient will often feel transient
for an arterial rupture or dissection, which may
require immediate attention.
7. The patient is given systemic heparin prior to stent
development of thrombus during the procedure.
8. After the procedure, the arterial access site is man-
use of a closure device (see Chap. 8 for more infor-
mation) after removal of the vascular sheath.
Post-procedural Care
After the PTRA or renal stent procedure, the patient may
experience a drop in blood pressure due to alleviation of the
RAS physiology and require vigorous intravenous hydration,
especially in young patients with RAS due to FMD.After the
procedure, patients may require blood pressure medication
adjustments for a period of 6weeks to 6months. The treated
renal artery will undergo gradual remodeling (Fig. 26.10,
Advancements in noninvasive vascular imaging technology
have resulted in an ability to more easily assess vascular
anatomy. However, we do not have an understanding of the
physiologic impact of a RAS detected incidentally on an
imaging study, nor do we have any correlative predictive
indices or biomarkers. What we do know is that not all
patients have clinical or laboratory sequelae related to a RAS
and that ARAS should be considered one aspect of systemic
atherosclerosis. Therefore, patients with ARAS should have
medical therapy for CV risk factor reduction to improve
morbidity and mortality outcomes. In contrast, patients with
FMD of the renal arteries, especially younger patients with
recent onset of hypertension, are more likely to approximate
the Goldblatt model of RVH, have less input from a systemic
inammatory process, and can be cured by a PTRA procedure [1–3].
Once a hemodynamically signicant RAS is felt to be a
contributing factor to hypertension, renal dysfunction, and/
or episodes of ash pulmonary edema in a patient without
signicant proteinuria, PTRA (for FMD) or stenting (for
ARAS) may be very benecial [12, 13, 19, 21–24].
Longitudinal care of these patients is required due to a
dened rate of recurrence of the RAS after PTRA for FMD
and development of in-stent restenosis after renal stent placement. In addition, patients with ARAS need ongoing assessment for progression of atherosclerosis and CV disease, and
patients with FMD need to be followed to ensure other vascular beds involved with FMD are managed or screened on
an ongoing basis [4, 9, 10].