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1、AcuteRenalFailure：GuYongDivisionofNephrologyHuashanHospitalAffiliatedtoFudanUniversityARF1.Definitionandconcept2.Pathogenesis3.Pathologyandpathophysiology4.Acutetubularnecrosis5.SpecialtypeofARF6.HandlingofARFDefinitionofARFSyndromeQuickdeclineofGFRAseriesofcli
2、nicalmanifestationAccumulationofnitrogen-containingtastesIncidenceofARFCommonhospitalization：5%ICU：>30%HouSHetal.AmJMed.1983；74：243FeaturesofARFKidney：completerestorationoffunctionHighincidenceofcomplicationHighmorbidity&mortalityOtherorgansdamageClassification
3、ofARFPrerenal：Hypoperfusion,functionality：55%-60%Renal：35%-40%Postrenal：urinarytract：5%CausesofprerenalARFLowvolume:bleeding,lostfromG-I,kidney,skin,thirdspaceLowcardiacoutput:myocardium,valve,Systemicvasodilatation:medicine,infection,allergy,liverfailureRenala
4、rterialsystole：shock,medicine,liverfailureRenalARFRenalgreatvesselsGlomeruleAcutetubularnecrosis：ischemia/poisoningTubulesandinterstitiumPostrenalARFPosition:UreterbladderneckAnteriorurethraCause：Stone,coagulatedblood,Crystal,edema,deligationTumor,fibrosis,sten
5、osis,prostateglandetc.ATNPathologyPathophysiologyCourseofdiseaseDiagnosisanddifferentialdiagnosisComplicationDeclineofGFRinARFAbnormalrenalhemodynamicsTubularimpairment:obstruction,backflowFactorsinvolvedinrenalhemodynamicsEndothelin：increasingreceptorblockingE
6、DNO：decreasingOthers：PlateletActivatingFactor(PAF)AdenosineMedullaedemaTubuloglomerularfeedback:TGFTubularimpairmentObstruction：CaducousepithelialcellsandcomponentsCastBackflow:ImpairedintegrityofepithelialcellsAccordingtohistology:tubularcellsfalloffandnecrosi
7、s,castMetabolicchangeaftertubularcelldamageDecreasedATPCellularswellingIncreasedintracellularcalciumIntracellularacidosisActivationofphosphatidaseActivationofproteaseOxidativestressConsequenceofdamagedtubularcellsIntactSublethalDeath:Apoptosis/necrosisDependon:
8、differentsite,toxinconcentration,timeNecrosis＆ApoptosisinARFNecrosis：cellularswelling,chondriosomechangeDestroymembranousIntegrityReleaseproteinlysaseperipheralcelldamage/in
