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内科学急性肾衰竭顾勇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
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