內(nèi)科學(xué)-急性腎衰竭顧勇

內(nèi)科學(xué)急性腎衰竭顧勇ARF1.Definitionandconcept2.Pathogenesis3.Pathologyandpathophysiology4.Acutetubularnecrosis5.SpecialtypeofARF6.HandlingofARFDefinitionofARFSyndromeQuickdeclineofGFRAseriesofclinicalmanifestationAccumulationofnitrogen-containingtastesIncidenceofARFCommonhospitalization：5%ICU：>30%；74：243FeaturesofARFKidney：completerestorationoffunctionHighincidenceofcomplicationHighmorbidity&mortalityOtherorgansdamageClassificationofARFPrerenal：Hypoperfusion,functionality：55%-60%Renal：35%-40%Postrenal：urinarytract：5%CausesofprerenalARFLowvolume:bleeding,lostfromG-I,kidney,skin,thirdspaceLowcardiacoutput:myocardium,valve,Systemicvasodilatation:medicine,infection,allergy,liverfailureRenalarterialsystole：shock,medicine,liverfailureRenalARFRenalgreatvesselsGlomeruleAcutetubularnecrosis：ischemia/poisoningTubulesandinterstitiumPostrenalARF

Position:UreterbladderneckAnteriorurethraCause：Stone,coagulatedblood,Crystal,edema,deligationTumor,fibrosis,stenosis,prostateglandetc.ATNPathologyPathophysiologyCourseofdiseaseDiagnosisanddifferentialdiagnosisComplicationDeclineofGFRinARFAbnormalrenalhemodynamicsTubularimpairment:obstruction,backflowage,multi-organinvolvedNoperipheralcelldamageandinflammationRenaleffectiveperfusionIncreaseGFR:expansionofafferentarterioleofglomerulus/increasedkfUremicpericarditisSurvivalrateNephrologist,UrolandRadiol：WorkhandinhandNecrosis＆ApoptosisinARFapoptoticbody→phagocytosisBackflow:ImpairedintegrityofepithelialcellsNormalfreethyroxinePosition:IncidenceofARFQuickdeclineofGFRDependon:differentsite,toxinconcentration,timeFactorsinvolvedinrenalhemodynamicsEndothelin：increasingreceptorblockingEDNO：decreasingOthers：PlateletActivatingFactor(PAF)AdenosineMedullaedemaTubuloglomerularfeedback:TGFTubularimpairmentObstruction：CaducousepithelialcellsandcomponentsCastBackflow:ImpairedintegrityofepithelialcellsAccordingtohistology:tubularcellsfalloffandnecrosis,castMetabolicchangeaftertubularcelldamageDecreasedATPCellularswellingIncreasedintracellularcalciumIntracellularacidosisActivationofphosphatidaseActivationofproteaseOxidativestressConsequenceofdamagedtubularcellsIntactSublethalDeath:Apoptosis/necrosisDependon:differentsite,toxinconcentration,timeNecrosis＆ApoptosisinARFNecrosis：cellularswelling,chondriosomechangeDestroymembranousIntegrityReleaseproteinlysaseperipheralcelldamage/inflammationApoptosis：Activeenergyconsumptionprocesscellnucleusshrinkage→smallDNAfragmentcellmembrane：blebbingbutintegrityapoptoticbody→phagocytosisNoperipheralcelldamageandinflammationDependonseverityofimpairmentRepair,RegenerationandRecoveryRecoveryofSublethalcellsScavengenecroticcellsandintracavitarycastsRegenerationofepithelialcells:replacenecroticandcaducouscellsTubularepithelialcellsintegrityandfunctionrestorationCourseofATNInitiation:noparenchymaimpairmentMaintenance:parenchymaimpairment:1-2weeks,maybe11monthsRecoveryPerspectivestudy：notprovedQuickdeclineofGFRAnti-ICAM-1EndothelinreceptorantagonistDependon:differentsite,toxinconcentration,timeRecoveryofSublethalcellsClassificationofARFWoundinfectionsPeritonealdialysisMyocardialinfarctionPostrenalARFVolumecontrol/toxincleaningcellmembrane：blebbingbutintegrityActivationofphosphatidaseFactorsinvolvedinrenalhemodynamicsDiagnosisanddifferentialdiagnosisofATNDiagnosis:medicalhistory,physicalexamination,UrineAnalysis,bloodtestOtherexaminationspastmedicalhistory,drughistoryDifferentialdiagnosis:AcuteorChronicClassificationCausesSpecialtypeofARFTumorRenaltransplantationPregnancyLungdiseasesOperationonvesselsofheartLiverdiseasesNephroticSyndromeDrugsWhykidneyeasytobedamagedbydrugs?Largevolumeofbloodflow:25-30%heartstrokevolumeActivemetabolismLargestendothelialcellsurfaceRichenzymaticsystemTranscellulartransportConcentrationfunctionMuchoxygenconsumption,littleoxygensupply(medulla)ComplicationofARF(1)MetabolicHyperkalemiaMetabolicacidosisHyponatremiaHyponatremiaHyperphosphatemiaHypermagnesemiaHyperuricemiaCardiovascularPulmonaryedemaArrhythmiasPericarditisPericardialeffusionHypertensionMyocardialinfarctionPulmonaryembolismPneumonitisGastrointestinalNauseaVomitingMalnutritionGastritisGastrointestinalulcersGastrointestinalbleedingStomatitisorgingivitisParotitisorpancreatitisComplicationofARF(2)NeurologicNeuromuscularirritabilityAsterxisSeizuresMentalstatuschangesSomenolenceComaHematologicAnemiaBleedingInfectiousPneumoniaWoundinfectionsIVinfectionsSepticemiaUrinarytractinfectionOtherHiccupsDecreasedinsulincatabolismMildinsulinresistanceElevatedPTHReduced1,25-dihydroxy-and25-hydroxycitaminDLowtotalT3/T4NormalfreethyroxineHandlingofARF（1）PrerenalRenaleffectiveperfusionFluidsupplement:Wholeblood,plasma,crystalfluidHeart:volumeload,arrhythmiaCirrhosisOthersHandlingofARF(2)Renal：Prevention：Prerenalfactors:volume,cardio-respiratoryfunctionUseofdrugsEspeciallyVasoactiveagentDiureticOthersNecrosis＆ApoptosisinARFIncreasethevolumeEndothelinreceptorantagonistClassificationofARFVasoactiveagentDifferentialdiagnosis:AcuteorChronicMyocardialinfarctionEDNO：decreasingcellnucleusshrinkage→smallDNAfragmentRepair,RegenerationandRecoveryLargestendothelialcellsurfaceAnti-ICAM-1Obstruction：FactorsinvolvedinrenalhemodynamicsIncidenceofARFDopamine1-3ug/kg/minIncreaseRPFandGFRPerspectivestudy：notprovedArhythmia/myocardialischemiaANPIncreaseGFR:expansionofafferentarterioleofglomerulus/increasedkfInhibitsodiumtransport,decreaseoxygenconsumptionExperimentsshowedeffectiveNotclinicallyconfirmedDiureticLargedoseDecreasevolumeloadMortalityanddialysisrateunchangedMannitol：NoclinicalevidenceIncreasethevolumeLowsodium（shift）OthersGrowthfactor:Insulin-LikeG-FEndothelinreceptorantagonistRGDpolypeptide:inhibittubularobstructionATPsupplementScavengeROSLeukocyteadhensioninhibiting：Anti-CD18Anti-ICAM-1Anti-P-selectinONRESEARCHNOWSpecialtreatmentofARF(notATN)CorticosteroidImmunosuppressiveagentPlasmapheresisAntiplateletBloodpressurecontrolComplicationtreatmentMetabolism：water-electrolyte,acid-basebalanceNutritionAnaemiaDialysisQuestions：Prognosis？Style？Dosage？Indication？DialysisPeritonealdialysisAcuteintermittenthemodialysisChroniccontinuoushemofiltration/hemodialysisCrystal,edema,deligationCourseofATNDependonseverityofimpairmentSpecialtreatmentofARF(notATN)WoundinfectionsConsequenceofdamagedtubularcellsCausesofprerenalARFapoptoticbody→phagocytosisTubularimpairmentCardiovascularfunctionunstableEndothelinreceptorantagonistAnti-ICAM-1Principle：TorelieveobstructionassoonaspossibleAccumulationofnitrogen-containingtastesHyperphosphatemiaDialysisAbsoluteIndicationsOliguria,urinaryvolume<500ml/dAnuria,>12hBUN>30mmol,Scr>1000μmol/LPneumonedema,noresponsetodiureticUremicencephalopathyUremicpericarditisIndicationo