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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3751_Библиотеки_им_академика_М_И_Перельмана
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relativelyfrequentfinding,particularlyintheolderpopulationwhomayhaveconcomitantatherosclerotic
disease in other vascular distributions. Yet most structural renovascular disease that may be visible
angiographically does not cause hypertension (renovascular hypertension) or renal ischemia as large
angiographicserieshavedemonstrated,withrecentmajortrialevidenceshowingthatoptimizedmedical
therapy rather than mechanical intervention may be appropriate in most cases. However, a subset of
individuals who have resistant hypertension,1 advancing renal dysfunction (especially with bilateral
disease),2orflashpulmonaryedemashouldbeidentifiedandtreatedbyrevascularization.
3
II.AnatomicConsiderations
Inmostcases,thereisasinglerenalarterybilaterally(typically5-7mmdiameter),withoriginsattheL1L2leveloftheaorta,eachdividingintosegmental,lobar,interlobar,arcuate,andinterlobularbranches.
4
In a minority ofcases, anatomic variationsmayincludedualrenalarteries,accessoryrenalarteries,or
early segmental branching renalarteries.5Whenthe main renalartery is occluded,potential collateral
sources(intercostal,lumbar,internaliliac,andadrenalarteries)mayprovideimmediateviabilitybutnot
long-termpreservationoffunctioningrenalmass.
4,6
III.PathophysiologicFactorsandNaturalHistory
A.SystemicHypertensionCausedbyRenovascularDisease
The mechanism of systemic hypertension caused byrenovascular disease was firstelucidated in 1934
through Goldblatt’s experimental renal artery clamping models7 and is founded upon reduced renal
perfusionpressureleadingtoactivationoftherenin-angiotensinsystemwithconsequentreleaseofserum
renin and angiotensin II. Renin is released in response to diminished perfusion pressure at the
juxtaglomerularapparatusoftheafferentrenalarteriolesandinresponsetoreducedsodiumandchloride
deliverytothemaculadensasegmentoftheascendingloopofHenle.8Inturn,systemicvasoconstriction,
sympathetic activation, and aldosterone-mediated depression of sodium excretion with consequent
volumeexpansionwillfollow.
B.PulmonaryCongestion
1.Thesepathologicadaptationscanpromotesuddenpulmonarycongestion(flashpulmonaryedema)and
mayexacerbate myocardial ischemiain vulnerable individuals.Locally, efferentarteriolar constriction
governedbyreleaseofangiotensinIIactsasacompensatoryresponsefavoringcontinuedrenalperfusion
and explains why in the setting of significant bilateral disease (or unilateral disease in a uninephric
individual),therewillbeariseinserumcreatininewhenantihypertensivepharmacologicinhibitorsofthe
renin-angiotensinsystemareused.Ontheotherhand,whenunilateraldiseaseispresent,inhibitorsofthe
renin-angiotensin system may be very useful in controlling hypertension (caused by activation of the
renin-angiotensinsysteminrenovascularhypertension),withoutariseinserumcreatinine,providedthat
thecontralateralkidneyishealthyandthatfunctionalrenalmassispreserved.
9
2.Theabnormalvasoconstrictedaswellasvolume-expandedpathophysiologicstateoftruerenovascular
hypertensionhighlightstheimportanceofcombinedvasodilator anddiuretictherapyfor pharmacologic
management.
8
C.LateRenalIschemiaandDysfunction
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Itisinterestingtoconsiderthatlaterenalischemiaanddysfunctionmaybefoundeduponseveralfactors
beyond simple reduced arterial blood flow, given that the kidney has relatively minimal oxygen
requirements.
10,11
Theseextraischemicfactorsmayencompassdirecthypertensiveinjurytobothischemic
and unaffected kidney, distal atheroembolic phenomena, and the generation of angiotensin II–based
profibroticmediators(transforminggrowthfactor-beta[TGF-β],nuclearfactor-kB,andplatelet-derived
growthfactor[PDGF]).
4,12,13
Restoringrenalarterybloodflowalonethroughreliefofstenosismaynotbe
enoughtoreversemanyoftheselatechanges.
14
D.AtheroscleroticRenovascularDisease
1.Theprogressivenatureofatheroscleroticrenovasculardiseaseisunderscoredbyseveralseriesthat
showed significant rates of progression of stenosis as well as occlusion by angiography or duplex
ultrasound:progressionin44%ofindividualsandocclusionin16%at4years,15progressionin11%of
individualsat2.6years,16andprogressionin35%ofindividualsat3yearsand52%at5years(49%at
3yifthebaselinestenosiswas>60%).
17
2.Untreatedseverediseasewithreducedrenalbloodflowmayleadtotheischemiclossoffunctioning
renalmass and hasbeenlinkedtogreaterdegreeofstenosisandhigherblood pressure.18In asecond
series,at1yeartherewasatleasta1.0cmreductioninkidneysizein13%ofsubjectswithunilateral
diseaseandin43%ofsubjectswhohadbilateraldisease.
19
3. Overall, renovasculardiseaseisamarkerforpoor long-term outcomes,
20
withfarworse five-year
survival in a recently surveyed community congestive heart failure cohort when compared with those
subjectsfreeofrenovasculardisease.
21
IV.ClinicalPresentations
A.Literature
Themedicalliteraturesupportsasignificantassociationbetweenrenovasculardisease(typicallydefined
as structural anatomic lesions greater than 50% stenosis diameter) and classical Framingham
atherosclerotic riskfactors (smoking,diabetes, hyperlipidemia, age), as well as aortic and peripheral
vasculardisease(38%)andcoronaryarterydisease(6.3%-23%),witha7%prevalenceofrenovascular
diseaseinthegeneralolderpopulation.
3,4,22,23
Acorrelationhasbeennotedbetweenrenovasculardisease
andtwo-tothree-vesselcoronaryarterydisease.24Longitudinalstudiessupporttheprogressivenatureof
renovasculardiseaseasnotedabove,especiallywhenlesionsareinitiallyfoundtobesevere,butithas
been pointed out correctly that most of these retrospective as well as prospective series predate the
inceptionofidealmedicaltherapies(aspirin,clopidogrelandothernovelantiplateletcompounds,statins,
modern antihyperglycemic agents, renin-angiotensin-aldosterone inhibitors) and lifestyle interventions
(diet andweightcontrol, exercise, sodium restriction,andsmoking cessation).4 This observation also
shedslight on why optimizedmedical therapy has proved equallyeffectiveas revascularization in the
most recent randomized prospective trials.25 Presence and severity of renovascular disease is also
associatedwith all-causelong-term mortality, likelyreflecting theadverse implications of generalized
systemicatheroscleroticvasculardisease.
26
B.Population
Thetrueprevalenceofrenovascularhypertensionis less than 1%inthe generalpopulationbutmaybe
muchhigherinstatesofresistanthypertension
27-29
orinthepresenceofothersuggestiveclinicalfeatures
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listedbelow(7.3%of837ofsuchpatientshadatleasta70%stenosisofoneorbothrenalarteries).
30,31
Clinical indicators of physiologically significant renovascular disease include (1) multidrug-resistant
hypertension
1,32
ormalignanthypertension(GradeIIIorIVKeith-Wagenerretinalchanges[hemorrhages
andexudates,papilledema,respectively]havebeenassociated)orthe rapid acceleration ofpreviously
well-regulated hypertension,33 (2) disparity in renal size or the presence of an atrophic (ischemic)
kidney,(3)riseinserumcreatininefollowingadministrationofinhibitorsoftherenin-angiotensinsystem
(suggestingbilateraldiseaseorunilateraldiseaseinsinglekidney),or(4)suddenunexplainedpulmonary
edemaormedicallyrefractoryanginapectoris.Onsetofhypertensionataveryyoungoraveryoldage
mayalso provide acluetosignificant renovasculardisease (Table8.1). The finding ofa systolic and
diastolicabdominalbruitradiatingtotheflankmaybeofcontributoryinterest,yetasaphysicalsignlacks
highsensitivityorspecificityforthediagnosisofphysiologicallysignificantrenovasculardisease.
Table8.1
ClinicalIndicatorsFavoringaSearchforRenovascularHypertension
Onsetofseverehypertensionatextremesofage
Lossofregulationofpreviouslywell-controlledhypertension
Multidrug-resistanthypertension
Tobaccouse
Atheroscleroticdiseaseinmultiplevasculardistributions
Unexplainednewrenalimpairment
Unexplainedflashpulmonaryedema
Refractoryangina
Malignanthypertension,includingretinalhemorrhages,exudates,andpapilledema
Disparityinkidneysize
Riseinserumcreatinineafterinceptionofrenin-angiotensinsystem-inhibitingtherapy
V.AtheroscleroticRenovascularDisease
A. It is estimated that atherosclerotic disease underlies renal artery stenosis in 90% of cases.
27
Nonatheroscleroticcauses,themostfrequentbeingfibromusculardysplasia,arereviewedbelow.Inmost
cases, the presence of structural atherosclerotic renovascular disease is not the cause of hypertension
(renovascular hypertension) or ischemia of the kidney, and historically most catheter-based
revascularizations that were performed without goodevidencefavoring truerenovascularhypertension
did not afford benefit.34 In parallel with this observation, recent trial evidence, presented below,
indicatesthatpatientswhohavewellcontrolledhypertensionandnormalrenalfunctionshouldbetreated
conservatively.Yetresistanthypertension,flashpulmonaryedema,orprogressiverenalimpairmentwith
renal ischemia (especially in the context of bilateral disease), may require revascularization, thus
improvingclinicalmanagementandpreventingtheneedforrenalreplacementtherapy.
35,36
B. Because there is considerable clinical overlap among states of (1) essential hypertension, (2)
renovascularhypertension,(3)anatomic renalarterystenosis,(4)diabetic nephropathy,and(5)chronic
renalimpairment,methodsofassessingthefunctionalsignificanceofanatomicrenalarterydiseasewill
assumeimportance,asnotedbelow.
37,38
Alternatively,althoughproteinuriaisafeatureinmanyformsof
renaldiseaseincludingischemia,renaldiseaseunrelatedtostenosismaybereflectedinanactiveurinary
sediment(typicallyacellularinthesettingofrenalischemia).
4,39
Additionally,elevatedcreatinineinthe
settingofunilateral stenoticdisease suggestsnonstenotic etiologiesbecausea single remaining healthy
contralateral kidney thatiswell perfused willmaintaina normalcreatininevalue.27However,a rapid
riseinserumcreatininemayportendabetterresultpostrevascularization,suggestingreversibility.
4,33
Of
note, a group of investigators has reported a 24% prevalence of severe atherosclerotic renovascular
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diseaseinend-stagerenaldiseasepatientsbeingconsideredfordialysis.
40
VI.NonatheroscleroticRenovascularDisease
A.FibromuscularDysplasia
1.Themostcommoncauseofnonatheroscleroticrenovasculardiseaseisfibromusculardysplasia,often
seeninyoungerwomenwhoarehypertensiveyetotherwisefree ofclassic atheroscleroticriskfactors.
One-thirdofcasesofrenalarteryfibromusculardysplasiaarebilateral,andthereisafamilialcomponent
aswellasageneticassociationwithpolymorphismsoftherenin-angiotensinsystem,specificallyhigher
frequencyoftheangiotensin-convertingenzyme(ACE)Iallele.41Ithasbeenproposedthat,becausethis
allele is linkedtolower circulating levels of angiotensin-convertingenzymeandpossibly lowertissue
levels of angiotensin II (which regulates vascular smooth muscle growth and synthetic activity), the
presence of the I allele may foster abnormal remodeling of the arterial media thus promoting
fibromusculardysplasia.
41
2.Unliketheatheroscleroticlesionwhichclassicallyinvolvestheaortaandostiumandproximalrenal
artery,afibromusculardysplasticstenosistendstoshowabeadedappearance(reflectingthetissuewebs
or baffles thatrestrictblood flow), and resides inthedistal two-thirds of themain renalarteryor its
principalbranches42(Fig.8.1).
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FIGURE8.1 Renovasculardisease:Fibromusculardysplasia.Diagnosticangiographyusinga5Finternal
mammaryarterycathetertoinjecttherightrenalarteryina67-year-oldfemalepatientwhodemonstratedthree-
drug-resistanthypertension.Procedurewasconductedviatherightcommonfemoralartery.Thereisaslight
inferiorangulationtotheoriginoftherightrenalartery.Notethebeadedappearanceofthemid-vesselconsistent
withfibromusculardysplasia.
CourtesyofJepthaP.CurtisMD.
3. Asdistinctfrom atherosclerotic renovascular disease, fibromuscular dysplasia rarelyprogresses to
total occlusion or ischemic nephropathy. In addition to predilection for young females, fibromuscular
dysplasticrenovasculardiseasehasbeenlinkedtotobaccoconsumption,alpha-1antitrypsindeficiency,
useofergotamine ormethysergide,pheochromocytoma, typeIVEhlers-Danlossyndrome,cysticmedial
necrosis, Alport syndrome, neurofibromatosis, and coarctation of the aorta.43 This species of
renovasculardisease respondswell tosimpleballoonangioplastyandexhibitsdurable results,without
theneedforintra-arterialstentplacement44(Figs.8.1–8.3).
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FIGURE8.2 Renovasculardisease:Fibromusculardysplasia.Followingadministrationof7000-u
unfractionatedheparin,usingatelescopingtechnique,a7Frenaldoublecurvesheathguidewasadvancedoverthe
5Finternalmammaryarterycatheter.Followingthefindingofa15mmHgmeangradientacrossthestenotic
region,angioplastywasperformedusinga4.0mmthena5.0mmballoontoamaximumpressureof6atm.
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FIGURE8.3 Renovasculardisease:Fibromusculardysplasia.Completionangiogramshowsfavorableresult,
revealing<20%residualstenosis.Subsequentclinicalcourseisnoteworthyforminimizationofantihypertensive
regimenandgoodpreservationofrenalfunction.
B.OtherRareNonatheroscleroticFormsofRenovascularDisease
Other rare nonatherosclerotic forms of renovascular disease include vasculitis, neurocutaneous
syndromes such as neurofibromatosis, Takayasu arteritis, aneurysms, congenital or posttraumatic
arteriovenous fistulae, congenital bands, postradiation changes, spontaneous dissection,
thromboembolization (typically cardiac in origin, from atrial fibrillation), atheroembolization, steal
syndromeinthesettingofceliacaxisocclusion,orthevascularcompressiveeffectsoflargerenalcysts,
pheochromocytoma, retroperitoneal fibrosis, or posttraumatic external scarring (Page kidney).
37,45
Regarding renal artery thromboembolization, there is scant experience reported in the literature
describingcatheter-basedtechniquesforrenalreperfusion,forinstancelocalthrombolysis.Posttransplant
renal vasculopathy, often appearing within 1 year of transplant, presents with renal impairment,
hypertension,andcirculatorycongestionandisbestmanagedwithangioplastyandstenting.
46
VIIDiagnosticExaminations
When clinical presentation is strongly suggestive of functionally significant renovascular disease,
noninvasiveassessmentisindicated,withseveralmethodseachharboringadvantagesanddisadvantages.
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A.RenalDuplexUltrasound
Renalduplexultrasoundisusefulwhengoodacousticwindowsareavailableinleanerindividuals.When
performedwelltechnicallyandinterpretedinacompetentmanner,thismethodcandefinekidneysizes,
charttheprogressionoflossofrenalmass, estimatethedegreeofechogenicityoftherenalcortex,and
illustrate the condition of the distal microvasculature. A physiologically significant stenosis may be
reflectedbyapeaksystolicvelocityof>200cm/sandarenalartery/aorticpeaksystolicvelocityratioof
3.5.47Renal resistive index (peak systolic velocity−end diastolic velocity/peaksystolic velocity) can
demonstrate the degree of microvascular resistance and may predict benefit of revascularization.
However, threshold values have not yet been fully defined in the literature,42 although 0.80
conventionallyhasbeentheupperlimitofnormal.Highervaluessuggestdistalmicrovasculardiseaseand
havebeenlinkedwithfailuretoimproveclinicallyfollowingmainarteryrevascularization.
48
B.CaptoprilRenalArteryScintigraphy
Captopril renal artery scintigraphyuses nuclear perfusionassessments before and after ACEinhibitor
stimulationtodeterminewhetherarterialflowisdependentonefferentarteriolarvasoconstrictionunder
theinfluenceofangiotensinII,thereforeconfirmingthatfunctionallysignificantrenovascularhypertension
is present.49 When comparing two kidneys, abnormal unilateral function may identify significant
renovasculardiseaseandpredictimprovementfollowingrevascularization.50However,whilespecificity
ishigh,sensitivitymaynotbeadequate,particularlyincasesofbilateraldisease(orunilateraldiseasein
a single kidney) or low glomerular filtration rate. There is little role for previous methods such as
intravenouspyelographyormeasurementofplasmareninactivity.Earlystudiesindicateapromisingrole
forassaysofbrainnatriureticpeptide(BNP,orB-typenatriureticpeptide)inpredictingbloodpressure
responsepostrevascularization.
51
C.Angiography
1. CT angiography may provide useful images, but radiation burden and nephrotoxic radiocontrast
exposurerepresentconcerns.Moreover,thistechniquemayfailtodistinguishintraluminalstenosisfrom
extravascularcalcification.42Stenosisof>75%(or50%withpoststenoticdilatation)maybeconsidered
significant.
2.MRangiographyisprobablythemostusefulcontemporarytechnique,requiringnoradiation,although
thereisafalsepositiverate.Astenosisof>80%maybeviewedassignificant.However,itsgadolinium
contrastagentmustbeusedwithgreatcautionwhenrenaldiseaseispresentgiventheriskofdevelopment
ofnephrogenic systemic sclerosis. Questions also surround the significanceoflong-term depositionof
gadoliniuminboneandbraintissue.
3. Invasive renal vein sampling for renin measurement has suboptimal sensitivity and specificity,
althoughlateralizingvaluespredicttreatmentresponse.
4. Percutaneous renal angiography carries the risks of any invasive catheter-based procedure
(bleeding, infection, embolization, vessel or kidney damage, radiation exposure, radiocontrast
requirement),yetprovidesexcellentimages,ishighlysensitiveandspecificforthedepictionofvascular
stenosis,permitsimmediatephysiologicassessments,andallowsballoonorstentrevascularizationinthe
same setting. Angiography is, however, relatively low risk and serves as the gold standard for
visualizationoftherenalarteries.
Femoral artery access is most commonly used, butupper extremity (radial or brachial artery) can be
employediftheoriginoftherenalarteryisangulatedinferiorly42orifthereismajorinfrarenalaortoiliac
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disease (Fig.8.1). Nonselective abdominal aortography performed at the T12-L1level uses a pigtail
catheter with power injection using dilute radiocontrast and digital subtraction angiography.47 The
nonselective view elucidates the presence and number of renal arteries, as well as important aortic
conditionssuchasprotrudingatheroscleroticplaquethatcouldinterferewithsubsequentselectiverenal
angiography.
42,47
Withadvancedrenalimpairment,carbondioxidemayactsafelyasacontrastmedium.
5.Intermsofangiographicviews,selectiverenalarteryangiographymayrequireaslightdegreeofleft
anteriorobliqueangulationgiventheanteriororiginoftherightrenalarterythatisslightlysuperiortothe
orificeoftheleftrenalartery,arisingmoreposteriorly.4Fromthefemoral approach,catheter selection
mayincludeinternalmammary(Fig.8.1),JR4,cobra,renaldoublecurve,hockeystick,multipurpose,or
SOSOmni.
42,47
Viaupperextremityapproaches,a90-cmlong6For7Fvascularsheathmayproveuseful,
throughwhicha5For6Finternalmammaryartery,multipurpose,orJR4cathetercanbeadvancedtothe
orificeoftherenalartery.
D.DiscoveryofStenosis
1. If a stenosis is discovered, determination of physiologic or functional significance may be useful
because there is a limited correlation between angiographic severity and functional significance,
particularly in the case of fibromuscular dysplasia.38 Simple measurement of translesional pressure
gradientmaybeuseful(Fig.8.4)yetisnotfullyinformative,however,becauseitdoesnotconsiderother
variablessuchasaorticpressure,cathetercaliber,potentialvasoconstrictedconditionofthedownstream
renal vasculature, and the ambient renal venous pressure (which could be elevated in many states,
including congestive heart failure)4 (Fig. 8.2). Translesional measurements can be accomplished by
placinga4Fcatheterdistaltothestenosis,comparedagainsta6or7Fguidingcatheter,whichwouldbe
locatedproximaltothestenosis.Becauseofitssmallersizeandthereforelesserpropensitytoincrease
artificiallythemeasuredgradient,a0.014pressurewiremaybepreferablehere.33Ithasbeensuggested
thatameantranslesionalgradientof10mmHgorapeak-to-peaksystolicgradientof20mmHgshould
beconsideredsignificantforintervention.
33
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FIGURE8.4 Renovasculardisease.Atheroscleroticrenalarterystenosis.Diagnosticangiographywas
performedviaatelescoping5Finternalmammaryartery/7Frenaldoublecurvesheathguideinthecaseofa65-
year-oldfemalewhosufferedwithdifficulttoregulateangina,labilehypertension,andultrasound-documented
progressivelossofrightrenalmass.Procedurewasconductedviatherightcommonfemoralartery,withdiscovery
ofa90%rightrenalarteryostialstenosis.A50%leftrenalarterystenosiswasfoundtohaveasystolicgradientof
<10mmHg,andwasthereforeselectedforoptimalmedicaltherapy.
CourtesyofMichaelS.RemetzMD.
2. Stimulated hyperemic gradients and fractional flow reserve (using pressure wire) can
pharmacologically eliminate distal vasoconstriction and, in a manner analogous to coronary lesion
functionalassessment,canprovideamoreaccuratepictureoflesionseverityandmaypredictresponseto
treatment.Inmostsituations,therenalfractionalflowreserveequalstheratioofthehyperemicpressure
distal tothe stenosisdividedbythe meanaorticpressuremeasuredbypressurewireevaluation.52 To
stimulatethehyperemicresponse,papaverine(30-40mgintra-arterial)hasbeenrecommended(andmust
be used with heparin-free saline toavoid an unwanted precipitate),andadenosineshould notbe used
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