【高血壓英文課件】Renovascular-Disease

RenovascularDiseaseMichaelShomaker,MDJanuary7,2003RenovascularDiseaseMichaelSh1GoalsDefinethoseatriskforRASandwhoshouldbescreenedReviewthepathophysiology,clinicalfeatures,andnaturalhistoryofRASandhowthiseffectstherapeuticdecisionsProvideabriefoverviewofthedifferentdiagnostictestsandtheirperformanceprofilesCriticallyreviewtheliteratureasitpertainstothedifferenttreatmentoptionsProvidehousestaffwithanevidence-based,practicalalgorithmfortheevaluationandtreatmentofRASatWakeForestAttempttopersuadeAlHadleyfrominundatingthehousestaffwithDukebasketballscoreseachdayatmorningreportGoalsDefinethoseatriskfor2【高血壓英文課件】Renovascular-Disease3【高血壓英文課件】Renovascular-Disease4【高血壓英文課件】Renovascular-Disease5NaturalHistory

MajorPointsARASisaprogressivediseaseARAShasbeenshowntobeassociatedwithrenalinsufficiencyPatientswithIRDthatprogresstoESRDhasadismalprognosisNaturalHistory

MajorPointsAR6NaturalHistory

CrowleyetalLargestcohortofpatientsevaluatingtheprogressionofARAS(1,189).Meanfollowupwas2.6yrsTheincidenceofsignificantstenosis(>50%)atbaselinewas6.3%NaturalHistory

CrowleyetalL7NaturalHistory

Crowleyetal.cont.Diseaseprogressionwasassociatedwithadeclineinrenalfunction.patientsinwhomstenosisprogressedfromnormalto>75%showedasignificantriseinserumcreatininecomparedwiththosewithlesssignificantprogression.Followupserumcreatininelevelinpatientswithnormalrenalfunctionatbaseline,categorizedaccordingtoprogressionofarterialstenosisNaturalHistory

Crowleyetal.8NaturalHistoryItisclearthatanatomicalARASisprogressiveinaproportionofpatients;however,ithaslikelybeenoverstated.Thevariablemostpredictiveofanatomicprogressionisthedegreeofinitialstenosis:PatientswithbilateralARASwithoneoccludedrenalarteryare3timesaslikelytoprogresstoESRDwithin2yearsthanthosewithbilateraldiseasewithoutocclusion(50%vs.18%)Therateoflossoffunctionalrenaltissue(impliedbyultrasoundevidenceofrenalatrophy)is3timeshigherinpatientswithbilateraldiseasethanforthosewithunilateraldisease(43%vs.13%).NaturalHistoryItiscleartha9PrognosisPatientswithIRDwhodoreachESRDdopoorly:HighestmortalityrateamongalletiologiesofESRD.2,5and10yearsurvivalratesare56%,18%and5%respectivelyMediansurvivalis25monthsMortalitylinkedtoCAD/CHFHowever,therecentprospectivecohortbyHansenetalshowedthatARAShadastrongindependenteffectonmortality(HazardRatio3.0)UnadjustedAdjustedPrognosisPatientswithIRDwho10PrognosisGiventhesepatients’dismalprognosisoncereachingdialysis,shouldwebeaggressivelytreatingthesepatients?PrognosisGiventhesepatients’11Pathophysiology

OverviewThepathogenesisofarterialatherosclerosisiswellunderstoodandratstudieshaveshownARASfollowsasimilarpattern.However,itisimportanttoreviewthemechanismsbywhichrenovascularhypertensionandIRDdevelop.Pathophysiology

OverviewThepa12Pathophysiology

OverviewIntraglomerularpressureremainsconstantduringwideswingsinsystemicbloodpressurebyalterationsinafferentandefferentglomerularvascularresistancesecondarytorenalautoregulation.RenalautoregulationfailstomaintainGFRwhenrenalperfusionpressuredipsbelow70-85mmHg,generallycorrelatingwithagreaterthan70%renalarterystenosis.Ithasbeenhypothesizedthatthiscriticalreductioninperfusionpressureisrequiredinordertosetoffthecascadeofeventsthatleadtorenovascularhypertensionand/orischemicrenaldisease.Pathophysiology

OverviewIntrag13Pathophysiology

RenovascularHypertensionPathophysiology

RenovascularH14Pathophysiology

RenovascularHypertension–UnilateralRASHighrenin,lowvolumeHigh/normalrenin,elevatedplasmavolumeIrreversibleparenchymalHTNThereseemstobethreephasesofhypertensionseeninpatientswithunilateralRAS:Pathophysiology

RenovascularH15Pathophysiology

RenovascularHypertension–UnilateralRASIrreversibleparenchymalHTN:ProlongedexposuretohighBPandhighlevelsofATIIcauseswidespreadarteriolardamageandglomerulosclerosisinthecontralateralkidney.ThisislikelywhyRVHsecondarytoARASdoesnotresolveafterrevascularization.HughesetalshowedthatcorrectivesurgeryforunilateralRVHwassuccessfulin78%ofthosewithHTNoflessthan5yearsdurationbutinonly25%ofthosewithHTNofalongerduration.Pathophysiology

RenovascularH16Pathophysiology

RenovascularHypertension–BilateralRASMuchlessisknownaboutthemechanismsofRVHinbilateralRAS.Theoverallpictureisamixedone,withbothreninandvolumefactorsplayingarole.Evidencesuggeststhereisanincreaseineffectivecirculatingbloodvolumeowedtoelevatedaldosteronelevelsandabluntedpressurenaturesiseffect.Pathophysiology

RenovascularH17Pathophysiology

IschemicRenalDiseaseSeveralreversible,adaptivechangesoccurinresponsetochronicrenalischemia:StructuralrenalatrophyDiminishedcorticalbloodflowReductioninGFRinordertodecreaseoxygendemandHypertrophyofthecontralateralkidneyHyperfiltrationoccursinthefunctionalnephronsofthenon-effectivekidney,whichleadstoglomerulosclerosis.Pathophysiology

IschemicRenal18Pathophysiology

IschemicRenalDiseaseItisverydifficulttoreliablydelineatetowhatdegreerenalinsufficiencyisduetoadaptivechangesvs.irreversibleparenchymaldiseasePathophysiology

IschemicRenal19ClinicalFeatures

OverviewThesepatientsdonotexhibitspecificclinicalfindings,anditisthereforeparticularlyimportanttoidentifyhigh-riskgroupsinwhichsuspicionofthisconditionshouldbeheightened.Therearetwoimportantischemicrenalsyndromestoconsider:ARFaftertheinstitutionofanACEIUnexplainedchronicand/orprogressiveazotemiaintheelderlywithevidenceofothervasculardiseaseMostofthesepatientshaveablandurinesedimentwithminimalornoproteinuriaandatrophickidneysonUSClinicalFeatures

OverviewThes20ClinicalFeaturesThefollowingclinicalfeaturesshouldraisethesuspicionofrenovasculardisease:YounghypertensiveptswithnofamilyhistoryornewonsetHTNinpts>50y/oAbruptonsetofHTNSevereorResistantHTNDeterioratingBPcontrolinlong-standing,complianthypertensivepatientsDeteriorationinrenalfunctionwithACEIEvidenceofsecondaryhyperaldosteronism(lowplasmapotassium,highrenin)Recurrent“flash”pulmonaryedemaandhypertensiveurgency(morecommonwithbilateralRAS)ElderlypatientswithPVDAbdominalbruit(OR11.5)Unexplainedrenalazotemia>1.5cmdifferenceinkidneysizeonUS(70%ofatrophickidneysintheelderlyareassociatedwithARAS)ClinicalFeaturesThefollowing21ClinicalFeatures

IschemicRenalDiseaseItisimportanttosearchforevidenceofunderlyingirreversibleparenchymalrenaldisease,asthissubgroupwillnotlikelybenefitfromtherapy.ModeratetosevereprotenuriaSevererenalatrophydistaltoobstruction

UnilateralRASwithrenalinsufficiencyClinicalFeatures

IschemicRen22Diagnosis

OverviewTherearetwogroupsofdiagnosticstudiesusedtoevaluateRAS:Anatomicstudies:Renalangiography–thegoldstandardDopplerultrasonographySpiralCTangiographyMRangiography Functionstudies:Renal-vein-reninmeasurementNuclearimagingwithI125iothalamateorDTPAtodetermineGFRConventionalrenographyACEIrenographyDiagnosis

OverviewTherearetw23Diagnosis

RenovascularHTNCaptoprilRenographyisanuclearstudywhichtakesadvantageofthefactthatACEIcanabruptlyreducerenalfunctioninanischemickidney.Patientsaregivenradio-labeledagentsthatareeitherexclusivelyfiltered(Tc99-DTPA),thusestimatingGFR,oragentsthatarefilteredandsecreted(Tc99-MAGorI131-hippurate),thusestimatingRBF.Abaselinestudyisdoneonday1and50mgofcaptoprilisgiven1hrpriortothesecondstudyonday2.Thedifferencebetweentheleftandrightkidneywithregardtouptake,excretion,kidneysizeandasymmetrycanbedeterminedbythisstudy.EitheraslowingoftheexcretionofTc99-DTPAorareductionoftheuptakeoftheTc99-MAGcanbeusedtoidentifytheeffectoftheACEIinremovingtheprotectiveactionsofhighlevelsofATIIontheautoregulationofGFRandonthemaintenanceofrenalbloodflow.Diagnosis

RenovascularHTNCapt24Diagnosis

CaptoprilRenographyDiagnosis

CaptoprilRenography25DiagnosisDiagnosticStudySens.Spec.PPVNPVRenalVeinRenins62%70-88%DopplerUltrasonography80-98%98%99%88-97%ConventionalRenography75%85%33%ACEIRenography75-90%94%92%88%CTangiography92%98%87%99%MRA100%93%90%100%DiagnosisDiagnosticStudySens.26Diagnosis

FunctionalstudiesDiagnosticStudyProsConsRenalVeinReninMeasurementsUsefulinconfirmingthefunctionalsignificanceofalesiondemonstratedbyanatomicalstudies–particularlyifbilateraldiseaseispresentPoorsensitivityNonlateralizationnotpredictiveofthefailureofHTNtoimprovewiththerapyNuclearImagingwithTc99-MAGorTc99-DTPAtoestimatefractionalflowtoeachkidneyAllowscalculationofsinglekidneyGFRand/orRBFDifficulttodifferentiatereversiblefromintrinsicdiseaseConventionalRenographyUsefulasbothascreeningtestandfunctionalstudyLowersens/speccomparedtoACEIrenographyACEIRenographyTestofchoiceforthediagnosisofRVHinmanycentersReducedsens/specinpatientswithrenalinsufficiency(Pcr>2.0)OperatordependentDiagnosis

FunctionalstudiesDi27Diagnosis

AnatomicStudies

“Ifyou’researchingforalesion,lookatthevessel.”DiagnosticStudyProsConsRenalArteriographyGoldstandardCanvisualizeaccessoryvesselsandintrarenalbrancheswellDirectcontrastloadtokidneysSometimesdifficulttodistinguishbetweencriticalandnon-criticallesionsDopplerultrasonographyNoninvasiveInexpensive;widelyavailableExtremelyoperatordependentDoesnotevaluateaccessoryvesselswellBowelgaspatterns/ObesityinterfereCTangiographyExcellentvisualizationofthevesselin3DHigh-contrastrequirementLessreliableforvisualizingdistalsegmentsandsmallaccessoryarteriesMRANoninvasiveProvidesexcellentimagesNon-nephrotoxic,thususefulinpatientswithrenalinsufficiencyExpensivePriorstentsproduceartifactsBloodflowturbulencecanexaggeratemeasuredstenosisDiagnosis

AnatomicStudies

“If28DiagnosisConventionalAngiographyofARASMRAofARASCTangiographyofARASConventionalangiographyofFMDDiagnosisConventionalAngiogra29Diagnosis

RecommendationsThediagnosticworkupofRVHorIHDshouldproceedasfollows:EvaluationofRVH:Ifthepatienthasnormalrenalfunction,thefirsttestshouldbeACEIrenographyorDopplerUS,basedonthelocalexperienceandequipment.Ifthistestispositive,ananatomicstudyshouldbeperformedtoconfirmthediagnosis,ifinterventionisbeingconsidered.EvaluationofIRD:DopplerUSisthetestofchoiceiflocalexpertiseadequatefollowedbyamoredefinitivestudytodelineatetheanatomyifinterventionisbeingconsidered.Ifnot:CTA/conventionalangiographyshouldbeperformedifRIismildMRAifRIismoderate/severeorduetodiabeticnephropathyDiagnosis

RecommendationsThed30Treatment

OverviewTodate,therehasbeennolargerandomized,clinicalcontrolledtrialcomparingmedicaltherapytonewerstentingproceduresorsurgery.Inaddition,mostofthereporteddataastotherapyhavebeennon-experimentalreports.Asresult,noimprovementsinsurvival,freedomfromdialysis,orprotectionfromadversecardiovasculardiseaseeventshavebeendemonstratedrelativetoanequivalentnon-interventionalcomparisongroup.Thus,IwillpresentasummaryofthemajorexperimentalreportsonPTRA/SandsurgeryTreatment

OverviewTodate,the31Therapy

RenovascularHTNTheEffectofBalloonAngioplastyonHypertensioninAtheroscleroticRenal-ArteryStenosis.VanJaarsveld,etal.NEJM,Apr.2000Objective

Thelong-termeffectsofrenalarteryangioplastyonRVHarenotwellunderstood.ThisstudywasconductedtodefinetheefficacyofangioplastyonRVH.Methods106patientsrandomizedtomedicaltherapyorangioplastyFollowupat3and12mo.PrimaryoutcomemeasureswasBPSecondaryoutcomemeasureswerenumberanddefineddailydosesofant-HTNmeds,Pcr,Clcl,andresultsofACEIrenographyThepts.inthedrug-therapygroupunderwent“rescue”balloonangioplastyif,after3months,theirdiastolicBPwas>targetdespite3ormoreanti-HTNmedsorifthecreatininehadrisenbymorethan0.2mg/dl.Intention-to-treatanalysiswasperformedTherapy

RenovascularHTNTheEf32Therapy

RVH-vanJaarsveld,etalTherapy

RVH-vanJaarsveld,e33Therapy

RVH-vanJaarsveldetal.RESULTS:TherewasnodifferenceinmeanBPbetweenthegroupsat3and12monthsThedoseofanti-HTNdrugsusedbypatientsintheangioplastygroupweresignificantlylowerthanthoseusedinthecontrolgroupat3months,butthisdifferencewasnolongersignificantat12months.HTNwasconsidered“cured”(goalBPonnoanti-HTNmeds)inonly7%oftheangioplastygroupTherapy

RVH-vanJaarsveldet34Therapy

RVH–vanJaarsveldetal.RESULTScont:Medianserumcreatininelevelsandcreatinineclearancedidnotsignificantlychangeineithergroup;howeverthefollowupperiodwasshort.Inthe22patientsrandomizedtothecontrolgroupwhocrossedoverandunderwent“rescue”angioplasty,statisticallysignificantimprovedbloodpressurecontrolwasseenpost-angioplasty.Inthetreatmentgroup,thepresenceofanabnormalACEIrenogramdidnotpredictbloodpressurecontrolafterangioplasty.Therapy

RVH–vanJaarsveldet35Therapy

RVH–vanJaarseveldetalStrengths:LargeststudytodateCarefulvalidationoftheradiographicdiagnosisofARASAdherencetoastricttreatmentprotocolWelldefinedpopulationwhowouldlikelybenefitfromintervention(mostlyunilateraldisease(78%),normal-mildrenalinsufficiency,evidenceofrenin-mediatedHTNwithabnormalACEIrenogram).Weaknesses:Almost50%ofthecontrolgroupcrossedover“critical”ARASwasdefinedas>50%ShortfollowupperiodwithnolongtermoutcomessuchasdeathorESRDStentsnotusedTherapy

RVH–vanJaarsevelde36Therapy

RVH–vanJaarsveldetal.Conclusions:Theresultsofthisstudyaredifficulttoevaluategiventhelargeamountofcrossover;however,thedataisconsistentwithothersmallerrandomizedstudies.ForpatientswhohaveRVHsecondarytoARASwithnormalormildlyimpairedrenalfunction,primaryangioplastywasnotmoreeffectivethanantihypertensivedrugsaloneforreducingbloodpressure.“Rescue”angioplastyfordifficulttocontrolRVHwasefficacious.AsfortheuseofPTRAinlimitingprogressionofIRD,thisquestioncannotbeascertainedfromthisstudygiventheshortfollowupperiod.ACEIrenogramhaslittleuseinthemanagementofRVHasitdoesnotpredictwhowillrespondtotherapy.Therapy

RVH–vanJaarsveldet37TherapyAlthoughthedataisnotentirelyclear,itappearsPTRAislikelynottheinitialtreatmentofchoiceforRVHsecondarytoARAS.Thus,attentionhasturnedtoassessinghowbesttoslowtheprogressionofischemicrenaldisease.Overthenextfewslides,Iwillreviewthebestoftheabundantnon-experimentalreportsonstentingproceduresandsurgeryforIRD.TherapyAlthoughthedataisno38Therapy

PTRAandPTRASStentplacementforRenalArteryStenosis:WhereDoWeStand?AMeta-analysis.Leertouweretal.Radiology;Jan.2000LargestreviewtodateevaluatingtheefficacyofPTRAandPTRASMethods:AllstudiesdealingwithPTRA(10articles;644patients)andPTRAS(14articles;678patients)between1991-1998wereselectedThepatientpopulationinthemajorityofstudiesweresimilar:(mildtomoderaterenalinsufficiency,age60-75y/o,renalinsufficiencyasindicationfortherapy)CriteriaforRASdidvariedamongststudies(>40to>70%)MostcriteriaforrenalimprovementwasPcrdecreaseby>20%Primaryoutcomemeasuresweresimilar(changeinrenalfunction,changeinHTNcontrol,angiographicpatency)PatientfollowupinmoststudieswasadequateTherapy

PTRAandPTRASStentpl39Therapy

PTRAandPTRAS–Meta-analysis#PatientsAgeProceduresuccessRestenosisRateComplicationsHTNcuredHTNimprovedRFimprovedRFStabilizedPTRA6446477%26%13%10%53%38%41%PTRAS6786698%17%11%20%50%30%38%Therapy

PTRAandPTRAS–Meta-40Therapy

PTRAandPTRAS–Meta-analysisFollowuprangedfrom6–48monthsThecriteriausedinmoststudiestodescribeBPimprovementwaspoor:Moststudiesconsidereda10mmHgreductioninSBPorDBPassignificantandmanypatientswhowere“cured”werestillonBPmeds.BPmedswerenotactivelyfollowedinthemajorityofstudies.Harm:7%inthestentgrouphadseverecomplications(ARF5%,renalinfarction1.3%,andperinephrichematoma1.3%werethemostcommon).StudiesusingPalmazstentshadasignificantlylowercomplicationrate(7%vs.25%)Overallmortalityratewas1%Therapy

PTRAandPTRAS–Meta-41Therapy

PTRAandPTRAS–Meta-analysisConclusions:PTRASappearstobeabettertechnicaltherapythanPTRAgiventhehigherinitialsuccessrateandlowerrestenosisrate.ThisisconsistentwiththeCVliteratureandislikelyrelatedtothefactthatmostARASlesionsareostialinnature.Stentplacementwasassociatedwithasignificantlylowerpercentageofpatientswithimprovedrenalfunction.However,thisislikelyduetothefactthatthebaselinePcrwashigherinthePTRASstudies.Thesestudiessuggestthat65-70%ofpatientsdohavestableorimprovedrenalfunctionafterPTRA/S.Therapy

PTRAandPTRAS–Meta-42Therapy

SurgeryCherretal(JVascSurg2002)recentlyreviewedtheclinicaloutcomesof626patientswhounderwentoperativerepairatWakeForestbetween1987-1999.LargestreviewtodateofthesurgicalmanagementofARASPatientpopulationhadahighburdenofvasculardisease:criteriaforARASwasstenosis>80%63%ofpatientshadbilateralARAS164RAOwerepresentin155patients41%underwentaorticormesentericreconstructioninadditiontoRArevascularizationThevastmajorityofpatientshadsevere,treatment-resistantHTN,andthiswasconsideredoneoftheindicationsforsurgery(avgBP200+/-35/104+/-21)PreoperativemeanPcrwas2.3withameanEGFRof40.5+/-23.2Therapy

SurgeryCherretal(J43Therapy

SurgeryRESULTS:RenovascularHTN->HTNwasconsideredcuredin12%andimprovedin73%IschemicRenalDisease->43%hadimprovementinEGFR(definedas>20%increase)and47%hadunchangedrenalfunction.Only10%didnotrespond.28patientswereremovedfromdialysisdependencefollowingsurgery!However,onfollowup,patientswithrenalfunctionunchangedbysurgerycontinuedtohaveaprogressivedeclineofrenalfunctionunchangedfrombeforetheoperation.Therapy

SurgeryRESULTS:44Therapy

SurgeryPerioperativemortalityratewas4.5%Complicationsoccurredin16%(HAP,arrhythmia,ARF,andMI)Significantindependentpredictorsofperioperativedeathincluded: HazardRatioAdvancedage(>70) 3.23ClinicalCHF 3.05AdvancedRI 2.35Diabetes 2.14Severeaorticdisease 1.69Therapy

SurgeryPerioperativem45Therapy

SurgeryConclusions:Thisnon-experimentalreportsuggestthat45%ofpatientshaveaslowingoftheprogressionoftheirIRD.RVH-SurgerydoesseemtoimproveRVHtoagreaterdegreethanPTRA/S,butitisnotclearwhetherthisdifferenceisclinicallysignificant.IRD-itdoesappearthatsurgeryismoreefficaciousthanPTRA/S;buttherearenolargerandomizedtrialstoconfirmthis.Giventhehighperioperativemortalityrate,thesurgicalriskisneedlessforthe55%whodidnotrespondtorevascularization.Therapy

SurgeryConclusions:46TherapySothisbegsthequestion->Aretherereliableclinicalpredictorsofwhowillrespondtotherapy?TherapySothisbegsthequesti47Therapy

IRD-Whowillrespondtotherapy?RapidDeclineinRenalFunctionReflectsReversibilityandPredicitstheOutcomeAfterAngioplastyinRAS.Murayetal,AJKD,1/2002Purpose–ToidentifyfactorsinfluencingclinicalsuccessafterPTRAMethods73patientswithIRD(Crcl<50ml/min)underwentPTRAforcriticalARASdefinedas>60%Therateofrenalfailurewasassessedbytheslopeoftheregressionlineofserumcreatinineversustime.ResponsewasassessedbycomparisonoftheslopebeforeandafterPTRA.42.5%hadbilateralRAS,and21.9%hadunilateralRASwithcontralateralRAOMeanfollowupwas627+/-284daysTherapy

IRD-Whowillrespond48Therapy

IRD–Whowillrespondtotherapy?Murayetal.AJKD,2002A:ptsw/slope<-0.00021Cr?=0.1mg/dl/moB:ptsw/slope>0.00013Cr?=-0.001mg/dl/moTherapy

IRD–Whowillrespond49Therapy

IRD–Whowillrespondtotherapy?RESULTS:58%ofpatientshadimprovementinrenalfunction,including3outof6whobecamedialysisindependentOnlytheslopeof1/Crwassignificantlyassociatedwithafavorabledeclineinrenalfailureprogression(p=0.004)SubacuteandrapidlyprogressiverenalfailureisassociatedwithafavorableresponseafterPTRA,astheyarelikelytohavelessparenchymaldiseaseTherapy

IRD–Whowillrespond50Therapy

IRD–Whowillrespondtotherapy?UseofDopplerUltrasonographytoPredicttheOutcomeofTherapyforRAS.Radermacheretal.NEJM,2/2001Purpose–Toevaluatewhetherahighlevelofresistancetoflowinsegmentalrenalarteriescanbeusedprospectivelytoselectappropriatepatientsfortreatment.Methods138patientswhohadeitherbilateral(47pts.)orunilateralRAS(91pts.)underwentPTRA/Sorsurgery.ClcrandBPweremeasuredbeforetheinterventionand3,6and12monthsandthenyearlyaftertheintervention.PatientsweregroupedbyasegmentalarteryRIof>80(35pts)or<80(96pts)Meanfollowupwas32+/-21monthsTherapy

IRD–Whowillrespond51Therapy

IRD–Whowillrespondtotherapy?*indicatesp<0.05Therapy

IRD–Whowillrespond52Therapy

IRD–Whowillrespondtotherapy?RESULTS:ForpatientswithRI<80andaCrcl<40ml/min,RIhasa95%sensitivityand85%specificityforpredictinganimprovementinrenalfunction.RI>80(p<0.001),Crcl<40ml/min(p=0.01),andmalesex(p=0.05)areindependentlyassociatedwithahigherriskofadeclineinrenalfunctionafterrevascularization.ThemeanrateofESRDat2years:50%forRI>80and5%foraRI<80.Therapy

IRD–Whowillrespond53Therapy

IRD–Whowillrespondtotherapy?Thus,itappearsclearthatafastrateofrenaldecline(>0.1mg/dl/mo)andRI<80arereasonableclinicalpredictorsofwhowillbenefitfromrevascularization.Therapy

IRD–Whowillrespond54Conclusions

NaturalHistoryandPathophysiologyARASisclearlyaprogressivediseaseTheinitialdegreeofstenosis/burdenofvasculardiseaseismostpredictiveofIRDprogression.OncepatientswithIRDaredialysisdependent,theirprognosisisextremelypoor.ThepathogenesisofIRDismultifactorial,andpredictingthedegreeofreversiblevs.irreversiblediseaseinaparticularpatientischallenging.HighRI,slowprogressionofIRD,significantproteinuriaandadvancedageseemtobepredictorsofirreversiblediseaseNormalRI,minimalproteinuria,andfastprogressionofrenalinsufficiencyseemtobepredictorsofreversiblediseaseConclusions

NaturalHistoryan55Conclusions

DiagnosisThediagnosisofIRDsecondarytoARASshouldbebasedonanatomicalstudies.FunctionalstudiessuchasACEIrenographyandrenal-vein-reninsamplingareinsensitiv