腎動(dòng)脈狹窄支架術(shù)現(xiàn)狀

Renalstentinginrenalarterystenosis

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腎動(dòng)脈狹窄支架術(shù)

patients發(fā)病率(%)Generalpeople0.1Hepertension1-5<50y,withHT(FMD)4-5>50y,wiht(ARAS)HT15CAD10-19criticalHT30HT+CAD20-30ESRD15-20HT+CAD+PVD40-60

HT+CAD+Renaldysfunction40-60Prevalenceofrenalarterystenosis(RAS)ARAS90%FMD10%

CommoncausesofrenalarterystenosisHTRenaldysfunctionAnginapectorisParoxysmalacutepulmonaryedemaPresentationofrenalarterystenosisHaemodynamics:

>50%

Renalperfusionpressurereduction

>70%

RPP<75-85mmHg,autonomicregulationlose

Pathology:Glomcrulus：arteriosclerosis,mesenteriumproliferation，Nephrictubule：epithelialcellsdenudation、apoptosis,Focalnecrosis，Renalinterstitium：Inflammatorycellinfiltration、fibrocyteproliferationEndstage：renalatrophyAtheroscleroticnephrosisNaturalcourseofARASstudyNF/U(mon)prograssion(%)Occlusion(%)Caps17033519Zierler80244811Tollefson4854539Schreiber85524416Developtototalocclusionwithin5years15%Deteriorationgraduallywithin5years

10-20%DeveloptoESRDannually5-15%3-yearmortalityinPt.withESRDondislysis50%SurvivalofARASPt.withESRDondislysis:5-year18%10-year5%AtheroscleroticRASprogressionConlonetal,KidneyInt2001Oct;60:490-7Renalangioin3987Pt.undergoingcath

IndependentpredictorofmortalityConlonetal,KidneyInt2001Oct;60:490-7Renalangioin3987Pt.undergoingcathIndependentpredictorofmortalityCase1:male，62y，HTCase2:male,78y，HT,DM,RenaldysfunctionRenalfunction:improement：GFRincrese15%/Scrdecrease0.2mg/dLstable：GFRchange<15%/Scrchange<0.2mg/dLineffective：GFRdecrease>15%/Scrincrease>0.2mg/dL

benefit：ImproementorstableBloodpressure:cure：SBP<140mmHgandDBP<90mmHg,withoutanyanti-hypertensiondrugs，improement：SBP<140mmHgandDBP<90mmHg,or,DBPdecrease>15mmHgwithsimilarorlessanti-hypertensiondrugsineffective：BPchangenotmeettheabovestandardbenefit：

cureandimprovementStandardforprognosisevaluationafterrenalarterystenting(Rundback)RenalarterystentingsuccessratestudyNProceduralsuccess(%)Burket127100Rodriguez10898Rocha15097QueenMaryhospital64100RuijinHospital12899PTRAonhepertensionstudyF/U(m)caursecure(%)Improve(%)Nochange（%)Lossino60FMDARAS571221512137Tegtmeyer39FMDARAS37256355020QMH34ARAS113257RJH6ARAS115633PTRAonrenalfunctionstudyNtechniquestable/improve(%)deterioration（%)Rodriguez105stent7228Rocha150stent928Steinbach222stent928QMH31stent8713RJH87stent6327Long-termeffectofstentingonRAS腎動(dòng)脈支架術(shù)治療腎動(dòng)脈狹窄患者的倪鈞張瑞巖胡健張憲鄭愛芳沈衛(wèi)峰上海交通大學(xué)附屬瑞金醫(yī)院心臟科（200025）摘要：目的:評價(jià)腎動(dòng)脈支架術(shù)治療腎動(dòng)脈狹窄的長期療效。方法:連續(xù)134例顯著腎動(dòng)脈狹窄患者接受腎動(dòng)脈支架術(shù)。記錄患者術(shù)前?術(shù)后24小時(shí)?1年和2年長期的血清肌酐（sCr），和血壓變化情況。結(jié)果:134例患者均成功置入支架，術(shù)后24小時(shí)肌酐較術(shù)前升高[（109.8±24.6）μmol/L比（99.4±27.8）μmol/L]，腎小球?yàn)V過率[（57.6±19.3）ml/min比（68.5±18.9）ml/min]較術(shù)前降低，但術(shù)后1年和2年的平均肌酐和術(shù)前比較差異無顯著性。腎動(dòng)脈介入治療術(shù)后6月，64例血壓得到改善。術(shù)后1年的平均血壓為（148.6±22.6）mmHg，與術(shù)前比較有顯著性意義。術(shù)后1年和2年分別有56例(50.9%)和50例(49.6%)患者獲益。結(jié)論:腎動(dòng)脈支架術(shù)治療腎動(dòng)脈狹窄的遠(yuǎn)期療效較好，且長期隨訪結(jié)果滿意。關(guān)鍵詞：動(dòng)脈粥樣硬化；腎動(dòng)脈梗阻；介入治療

WhysomePt.gainnobenefitfromRASstenting?RenalparenchymaimpairmentdiabeticnephropathyrenalimpairmentduetoHTrenalimpairmentduetoothersIschemicnephropathyAgeCINRestenosisfactorsInfluencingtheoutcomesin

RAS

underwentstent

nephron

redunctionvolume-dependenthypertension：(BilRAS/renaldysfunction)renin-dependenthypertension：(uniRAS)sympatheticnervoussystemvasoactivesubstancesecretedfromkidney：natriuretichormonevasopressinMechanismofhypertensioninCKDRenalarteriolarsclerosisinbenignhypertensionEarlystage：hyalinizationinafferentglomerulararterioleand

arteria

interlobularesadvancedstage：glomerulus,nephrictubule,renalinterstitiumdiseaserenalarteriolarsclerosisinmalignanthypertension(DBP>120mmHg)

Necroticarteriolitis,ProliferatingendarteritisPathologyofhypertension-inducedrenalimpairmentNephrosis

duttocholesterolcrystalembolizationEpidemiology：authorpopulationcasesincidence(%)FloryAortaAS2673.3Orossautopsy37222.4JonesUnexplainedrenaldysfunction2451.0Preston>65years3344.2etiologicalfactor：AS、endovascularprocedureHenry(Percusurge)AJCOct,2000TCT30RASof24Pt.(27ostial)Allhadrenalimpairement,71%hadHTSuccessrate100%Occlusiontime418sec(149-797)EmbolizationafterstentingEmbolizationafterstentingImprovedrenalfunction46%Unchanged4%Acutedeterioration0%Norenalfunctiondeterioretionat6month6/30(20%)empty24/30(80%)hadfiltercontentChronicthrombusCholesterolcleftsfragmentKidneyinelderlyKidneychange

vesselofkidney：renalarteriolarsclerosis

renalglomerulus：normaladult1.3million，1/3-1/2lostin70year-old

renaltubule：epithelialcellhypertrophia,renalinterstitium：atrophy,fibrosisRenalfunctionchange

renalbloodflow：10%redunctionper10years

GFR：Among40-80year-old,GFRdecrease0.8-1ml/minevery1year

KidneyinelderlyContrastinducednephrosis(CIN)AcuterenalimpairmentaftercontrastapplicationScrincrease>44.2μmol/LOr,increase>25%comparedtobaselinePrevalence:unselectedPt.:1-6%，Highrisk40-50%

RiskfactorsrelatedtoCINExistedrenaldysfunctionDMVasculardiseaseElderlyLowerEFhypovolemiadehydrationCongestiveheartfailurenephroticsyndrome;LiverCirrhosisBergKJ,ScandJUrol

Nephrol2000;34:317-322EffectofDMandrenalfunctionontheincidenceofCIN(n=1196）RI：renalimpairmentDM：diabetes

Rudnicketal.(1995)0510152025+RI+DM+RI–DM–RI+DM–RI–DM0%5.7%19.7%%0.6%EffectofDMandrenalfunctiononCINwithdifferentcontrastapplication0102030405060*定義為血清肌酐升高＞44.2μmol/l或＞25%（Laμtinetal.應(yīng)用的標(biāo)準(zhǔn)為＞26.5μmol/l或＞20%）**基線血清肌酐＞133μmol/l（Barrettetal.的研究中＞124μmol/l）Patients(%)VisipaqueOmnipaqueorthersAspelinetal.2003Manskeetal.1990Wangetal.2000Rudnicketal.1995Taliercioetal.1991Lautinetal.1991Barrettetal.1992Renalarterystenting

restonosisauthorscasesF/Urestenosis(%)Shammas1322-20月26Wienklin403.3年12.5Zeller1564年11.4IIkay2614.3Yutan88531QueenMaryhospital641212.5RuijinHospital1086-20月11.52006AHA/ACC

Guideline

IndicationsforRASRevascularization(a)Asymptoatic

Stenosis（ClassIIb）1.asymptomaticbilateralorsolitaryviablekidneywithahemodynamicallysignificantRAS.(Levelofevidence:C)

2.asymptomaticunilateralhemodynamicallysignificantRASinaviablekidneyisnotwellestablishedandispresentlyclinicallyunproven.(Levelofevidence:C)(b)Hypertension（ClassIIa）hemodynamicallysignificantRASandacceleratedhypertension,resistanthypertension,malignanthypertension,hypertensionwithanunexplainedunilateralsmallkidney,andhypertensionwithintolerancetomedication.(Levelofevidence:B)JVascIntervRadiol.2006Sep;17(9):1383-97

PreservationofRenalFunctionClassIIaRASandprogressivechronickidneydiseasewithbilateralRASoraRAStoasolitaryfunctioningkidney.(Levelofevidence:B)ClassIIbRASandchronicrenalinsufficiencywithunilateralRAS.(Levelofevidence:C)ImpactofRASonCongestiveHeartFailureandUnstableAnginaClassIhemodynamicallysignificantRASandrecurrent,unexplainedcongestiveheartfailureorsudden,unexplainedpulmonaryedema(Levelofevidence:B)ClassIIaPercutaneousrevascularizationisreasonableforpatientswithhemodynamicallysignificantRASandunstableangina(Levelofevidence:B)JVascIntervRadiol.2006Sep;17(9):1383-97

ClassIRenalstentplacementisindicatedforostialatheroscleroticRASlesionsthatmeettheclinicalcriteriaforintervention.(Levelofevidence:B)2.BalloonangioplastywithbailoutstentplacementifnecessaryisrecommendedforFMDlesions.(Levelofevidence:B)

JVascIntervRadiol.2006Sep;17(9):1383-97Catheter-basedInterventionsforRAS

BNPincreaseiscommoninpatientswithhypertensionSilvastudyBaselineBNP>80pgml77%PtsBPimprovedpostprocedure<80pgml0caseimprovedBNPdecresedafterprocedure>30％94％BPimproved<30％10％BPimprovedPredictorforRASstenting

DopplerwireFFR≦0.8BPandrenalfunctionimprovePressurewireDistalrenal/Aorta<0.9indicatehighreninlevel,BPimpreovedafterprocedureRI=(peaksystolicvelocity–enddiastolicvelocity)/pea