【持续性肾脏替代治疗crrt英文精品课件】acute kidney injury

AcuteKidneyInjury currentconceptsregardingdiagnosisandmanagement DavidA Makil M D KantorNephrologyConsultantsLasVegas NV AKICase 1 45y o malepresentstoERwithsubjectiveweightgain fatigue andvomiting HehadapreviouslynormalPEx serumchemistries3monthspriortocurrentpresentation CurrentlyhehasBP150 110 perorbitaledema LabsincludeBUN85 SCr9 0 UAshows2 protein blood andcellularcastsWhatstatementisleastlikelytobecorrect RenalbiopsyisindicatedPost strepGNisintheDDxExtracapillarycellproliferationislikelySpontaneousresolutionofthisparticularAKIislikelyHigh dosesteroidsareindicated AKICase 2 65y o malepresents7daysfollowingadiagnosticcoronaryangiogram symptomsincludeabdpainandconfusion PExrevealsdiminishedperipheralpulses livedoreticularis epigastrictenderness andalteredmentalstatus Labs BUN131 SCr5 2 UAshows10 15WBC 5 10RBC onehyalinecastperHPFThemostlikelydiagnosisis AINsecondarytoNSAIDSpttakingpost LHCRhabdomyolysiswithATNATNsecondarytoradiocontrastexposure nephropathyCholesterolembolizationRenalarterialdissectionwithprerenalazotemia AKICase 3 50y omaleisreceivingampicillinandgentamicinforthepast2weeksfortreatmentofenterococcalendocarditis Hehasremainedfebrile Labs Na145 K5 0 Cl110 HCO320BUN40 SCr3 5UA0 1WBC UrineNa20 Cr35Whichofthefollowingisthemostlikelyprocessimplicatedinthispatient sAKI AcutetubularnecrosisInsensibleskinlossesRenalarteryembolismDecreasedcardiacoutput CHFAcuteinterstitialnephritis AKICase 4 30y ofemalewithESRDsecondarytoDMnephropathyreceivesacadavericrenalallograft ByPOD 3 herSCris1 8mg dLonaregimenoftacrolimus prednisone mycophenolate OnPOD 5shedevelopsoliguria andtheSCrincreasesto2 2mg dL HerBPis160 80andstable temp37 2CThebestinitialstepinthispatient smanagementwouldbeto DecreasethedoseoftacrolimusObtainultrasonagraphyoftheallograftAdministerIVLasixandmonitorurineoutputEmpiricpulsesteroidtherapyObtainbiopsyofallograft AcuteKidneyInjury 2ndCenturyAD Galensurmisesurineformedfromkidneys330 1453AD ByzantinephysiciansdescribeoliguriaassymptomofAKI aswellasdetailedurinefindingsinAKI also thetransitiontopolyuricphaseaslatefindinginAKIisrecognized330 1453AD likelyprecursorstoATNdescribed Aetius thereasonsforthedestructionofthekidneyarethetoxicinfluenceofremediesandpoisons andexternalpressure Nonus hematuriaresultsfrompoisonousdrugsandserpentvenom EftychiadisAC AmJNephrol1997 AcuteKidneyInjury 1827 EnglishphysicianRichardBrightdescribesmicroscopichematuria oliguria andedemainacuteandchronicrenalinflammatorystates giveseponymicdefinitionforacute chronicGNFamousvictimsofBright sDisease ChesterA Arthur 21stU S PresidentLinusPauling NobelLaureateEmilyDickinson AmericanpoetCatherineEddowes victimofJacktheRipperAntoninDvorak CzechcomposerIsaacAlbeniz Spanishcomposer AcuteKidneyInjury WWI WWII Post traumaticoliguriaseenincombatants crushsyndromeevolvesasanAKIdx1950 1960 s AKIfoundretrospectivelyin 20 ofpost opopenheart aorticsurgery AcuteKidneyInjury WWI observationsofthirstandoliguriaincombatvictimsledtorelationshipbetweenblunttraumaandAKI Better OS1997 WWII SpanishsurgeonJosephTruetaobservessameinSpanishCivilWar WWIIcombatantsInducesrenalcorticalvasospasmexperimentally Trueta etal 1947 WWII BywatersandBealllinkmyoglobintoAKIincrushsyndromeduringLondonBlitz 1940 AcuteKidneyInjury AcuteRenalFailure ARF Traditionallydefinedastheabruptdecreaseofrenalfunctionsufficienttoresultinretentionofnitrogenouswasteproducts aswellaslossofregulationofextracellularvolumeandelectrolytesWhileconsensushistoricallyexistsinthisdefinition noneexistsregardingthequantificationofthisdeclineinfunctiontofullydenoteasARF AcuteKidneyInjury Creatinine SCr notsensitiveindetectingtheearlydeclineinGFRinearlystagesofARFNon steady stateofGFRvis visSCr CreatinineaccumulationlagsbehindRiseinSCrusuallyapost factofindingOliguria anuria statesmaynotexistevenwithsignificantdeclineinGFRStudiesofARFuseddifferentcriteriaforSCr SCrLackofconsensusproblematicalsowhenstudyingtheeffectsofinterventionforARFHou et al 1983 usedgradatedSCr SCrinprospectivestudyofhospital acquiredARF AcuteKidneyInjury 2001 AcuteDialysisQualityInitiative ADQI Risk 1 5xincinSCr GFRdec25 UOP4wksESRD completeloss incneedforRRT 3months2007 AcuteKidneyInjuryNetwork AKIN ModifiedRIFLEtoinclude SCro 3mg dLfrombaseline within48hr basedon80 mortalityrisk Chertow JASN2005 2007 AcuteKidneyInjuryproposedbyAKIN AcuteKidneyInjury AKIbetterrepresentsthefullspectrumofacutedisordersofrenalfunction especiallyinregardstoreversibleinjury Palevsky 2008 Issueofprerenal obstructiveetiologiesnotentirelyclearinAKIdefinition butclassicallyheldtoexistinthisframeworkDespitetheseattempts SCr oliguriatrendsstillsuboptimalinoutcomes treatmentmeasurementNeed Troponin analogue AcuteKidneyInjury PRERENAL AKI INTRINSIC POSTRENAL AcuteKidneyInjury PRERENAL 40 80 Volumeloss SequestrationImpairedCardiacOutputHypotension andpotentiallyhypo oncoticstates Netresult glomerularhypoperfusion AcuteKidneyInjury RENAL INTRINSIC 10 30 Vasculardisorders smallvessellargevesselGlomerulonephritisInterstitialdisorders InflammationintercalativeprocessesTubularnecrosis IschemiaToxinPigmenturia AcuteKidneyInjury POSTRENAL 5 15 IntrarenalCrystalsProteinsExtrarenalPelvis UreterBladder Urethra AcuteKidneyInjury PrerenalandATNencounteredmostofteninthehospitalsetting 70 75 inmanystudiesMostcommondiagnosticconsiderationisthereforebetweenthesetwoconditionsPrerenal IntravascularvolumedepletionHypotensionEdematousstatesLocalizedrenalischemiaATN Allcausesforprerenal leadingtopost ischemicATNToxins AKI Diagnosticstudies urine Urinalysisforsediment castsResponsetovolumerepletionwithreturntobaselineSCr24 72hrc wprerenaleventUrineNa FENaFENa UNaxSCrx100SNaxUCrFENa2 ATNHansel sstain UrinalysisinAcuteKidneyInjury PrerenalPostrenalOncoticAKI GlomerulopathyVasculitisThromboticMA PyelonephritisInterstitialnephritis AINAthero embolicAKI ATNMyoglobinHemoglobin UricacidToxinsDrugs Plasmacelldyscrasia HematuriaRBCcastsproteinuria WBCWBCcasts Eosinophils RTEcellsPigmentedcasts Crystalluria Non albuminproteinuria Abnormalsediment Normal bland AcuteKidneyInjury LABORATORYDATACreatinine alsoBUN CrratioCBC anemia thrombocytopeniaHCO3 aniongap lacticacid ketonesKCPK LDH Uricacid liverpanelSerologies ComplementESR RF ANA ANCA AntiGBMElectrophoresisToxicologystudies AcuteKidneyInjury IMAGINGSTUDIESUltrasound evaluatesrenalsize abletodetectmasses obstruction stonesCT detectsmasses stones caveatexistswhenIVCDisconsideredMRI MRA candetectRAS useofGadoliniumcarriesuncertainR BratioinAKI2 potentialhemodynamicchangessimilartoIVCD andNFDIntheAKIsetting U SprovidesmostinformationwiththemostfavorableR Bratio AcuteKidneyInjury PrerenalAzotemia fallinGFRsecondarytorenalhypoperfusionthatpotentiallyhasrapidreversiblecomponentRestorationofeffectiveintravascularvolume perfusionpressureBycurrentdetectablemethods AKIreverseswithminimalevidenceoftubularischemia AKI AcuteTubularNecrosis Non oliguricvs OliguricPrognosisworsewitholiguricATNinmostseriesIschemicinsult medullamostsusceptibletohypoxicevent cellularATPdepletion oxidativeinjuryAKI ARFphaseofATN 7 21daysonaverageRecoveryphaseofATN alsoknownasdiureticphaseHighurineoutput 3 4L K Mg PO4wastingAssociatedwithhighFENa AKI AcuteTubularNecrosis SalineloadingeffectiveinloweringATNriskfromdrugs pigments toxins sometimeslimitedinpost ischemicATN particularlyifCO CIcompromisedMaintenanceofCO BP avoidnewinsultsPreventativeagentshaveshownpromiseinanimalmodels butpoorlytranslatedtoclinicalsituationsDopamine fenoldopam mannitol statins loopdiueticsIdentificationofhighriskAKIpatientsisessentialtoprevention DM CKD ASCVD poornutrition AKI Rhabdomyolysis Precipitatedbytrauma crushinjury extremeexertion statins cocaine envenomation hypoK hypoPO4Multifoldinjury withvolumedepletion directtubulartoxicity andobstructingpigmentcastsUA granularcasts bldondipstickbut microscopyduetomyoglobinpigmentCKlevelsnotalwaysconsistentinpredictingAKI butgeneralconsensusisthatlowlikelihoodexistswithCKlevelslessthan5k 10k Rhabdomyolysis Endotoxincascade ActivationofETNOscavenging MuscularvasodilatationanduptakeofECFindamagedmuscles IncreasedloadofPO4andurate MyoglobinemiaHyperuricemia Hypovolemia CVsuppressionduetohiK loCa MetAcidosis MyoglobinuriaUricosuria Renalvasoconstriction ischemia Pigmentnephrotoxicity Tubularcastformationandstasis DepletionofATPstores synergistictubulardamage ATN ZagerRA KidneyInt1996 49 314 326 AKI Rhabdomyolysis Treatmentisviaforcedsalinediuresis goalofUOP 200 300mL hrEarlyhydration incrushvictims IVbeguninfield advisedevenbeforefullextrication Turkeyearthquake 1999 UrinaryalkanizationTreatmentforsymptomatichypocalcemiaonly watchforhyperK AKI RadiocontrastNephrotoxicity Well recognizedadverseoutcome butincidencevarieswidely becauseofproblemsindefiningAKIhistorically aswellascompetingfactorsinpathogenesisImprovedwithiso osmolaragentsOnsetofriseinSCroccurswithin24hr peak fallwithin3 5daysDdxofembolicAKI ATNfromothercausesManystudieswithdiuretics osmolaragents dopaminergicagents etc recentimprovementswithsaline HCO3pre postat1mL kg hrMucomysthasrecentequivocalbenefit butharmless Atheroembolic AE AKI RenalandsystemicAEoccurinpatientswithdiffuseatherosceroticdiseaseRiskfactorsincludemanipulationoftheaortaorotherlargearteriesduringangiographyorCVsurgeryAlsocanoccurspontaneouslywithulceratedplaquesDestabilizationofplaquemaybeenhancedinthesettingofanticoagulationorthrombolytictherapy AtheroembolicAKI ClinicalManifestationsAKIdaystoweeksaftermanipulation anticoagulationSystemicsigns signalsofinflammationRashLivedoreticularisDecreasedcomplementduetoactivationbyexposedatheromataEosinophilia eosinophiliuriaOcclusionofdistalarteriolarbedsAKIVisualfielddeficitsGangrenousdigits palpablepulsesPancreatitisGIbleeding AcuteKidneyInjury ClinicalfeaturesofAcuteInterstitialNephritisOnsetusually3 5dayswithmostdrugs butmaybesoonerwithrifampin ormuchlaterwithNSAIDSRisingSCrwhichresolvesupond cofoffendingdrugFever hematuria pyuria UrineeosinophilsMildtomoderateproteinuria muchhighertoNSinNSAIDSEosinophiliaandmorbilliformrashalsos sxinAINOccasionallyseehyperkalemiaanddistalRTABxnotusuallynecessaryfordx assumingreversalofsx s maybeneededforcomplicatedcasesPrednisone40mgPOx2wkssometimesutilizedtoshortenAKIinterval AcuteKidneyInjury AINcauses DRUGSACEIAllopurinolCephalosporinsCimetidineFluoroquinolonesLoopdiueticsNSAIDSPCNPhenytoinRifampinSulfonamidesTegretolThiazides INFECTIONBacterialAgentscausingpyelonephritisLegionellaBrucellaYersiniaViralHantavirusHIVCMV EBV HSV AKI Glomerulonephritis RPGN SystemicVasculitis Immune ComplexMediatedSLECryoglobulinemicvasculitisHenoch Sch nleinpurpuraPost strepGNDirectAbattackAnti GBMdiseaseGoodpasture ssyndrome Pauci immunevasculitisMicroscopicpolyangiitisWegener sgranulomatosisChurg StrausssyndromeThromboticMicroangiopathyTTPHUSSclerodermarenalcrisisPreeclampsiaMalignanthypertension AcuteGlomerulonephritis RPGN AccountsforaminorityofAKI 5 Mayhaveseveremorbidity mortailtyExtra renalmanifestationsmaybepresentPulmonaryDermalGIHematologicHTNmaybepresent especiallyinabsenceofpriorHxUA differentiatesfromATN AINDysmorphicRBC RBCcasts proteinuria 0 5gm 24hSerologies complementactivationNeedforspecifictherapytoreduceAbcriticaltowardsattenuating reversingAKI SystemicLupusErythematosus SLE SLEnephritisdiagnosisbasedonpathology serology extrarenalmanifestations 4 11criteriabyARAWHOClassI VofSLEnephritis histopathologyVariables sxofrenaldisease butClassIV diffuseproliferativeGN mostoftenseeninAKIANA anti DNAAb hypocomplementemiaRoleofBxtoguidetherapyImmunosuppressionSteroidscyclophosphamide Anti GBMdisease Goodpasture s PulmonaryhemorrhagedistinguishesGoodpasture sfromanti GBMdiseaseBimodalpeakincidence3rddecade men pulmonaryhemorrhagewithAKI Goodpasture s 6th 7thdecade women anti GBMAbAKI nopulminvolvementAbtargetstypeIVcollagenAggressivecourseofAKItypicallyseen pulmhemorrhageseenmoreofteninsmokers exposureAnti GBMpresentin 95 casesPredisonepluscyclophosphamide TPExindicateddailyuntilcirculatingAbtitersundetectable Pauci immunevasculitis Microscopicpolyangiitis Wegener sgranulomatosis Churg StrausssyndromeRBCcastswithproteinuria ESRelevated crescenticGNonBxRespiratorytractinvolvementmayvaryAlveolarhemorrhageSinusitis nodularlesions Wegener s Asthma eosinophilia Churg Strauss ANCAhallmarkofdiseasespectrum 90 MPO inmicroscopicpolyangiitis Churg StraussPR3 inWegener sPrednisone Cytoxan TPExusedinpulmhemorrhageRenalsurvivalassociatedwithentry levelSCr ThromboticMicroangiopathy Hemolytic uremicSyndrome Thromboticthrombocytopenicpurpura PredominatelyoccursinchildrenAssociatedwithdiarrhealprodrome Shigatoxin verotoxin E coliO157 H7Predominanceofuremicsigns symptomsHallmarkofendothelialdamagefromverotoxinSupportivecare PredominatelyinadultsNoincitingpathogen GIprodromePredominanceofCNSsigns symptomsHallmarkofcirculatingvonWillebrandfactor induceddamage defectinproteasePlasmaexchange AcuteKidneyinjury Crystal inducedAKI Commonfactorsincludehighexcretioninurine andlowsolubilityinacidicurine exacerbatedbyhypovolemia examinationofurinecriticaltoDxCommonagentsUricacidAcyclovirSulfaMethotrexateEthyleneglycolPre exposurehydration Urinaryalkalinization AcuteKidneyInjury IndicationsforRenalBiopsyinAKI TissueexaminationviaLM EM IFAcutenephriticsyndromeHematuria cellularcasts proteinuriainsettingofnew onsetorexacerbationofHTN risingSCrMayalsohaveserologic i e ANA ANCA aGBMthattissuedxalsoprovidestreatmentoptionsandprognosisUnexplainedAKIUncertainormultiplecompetingddx ofwhichtreatmentdiffersgreatlywithdefinitivedx AINvsATNconsiderationsareseennotuncommonlyinhospitalizedptsYoungptswithAKIoftenareconsideredbasedonlong termrenalsurvivaloutcomesmaximizedwithdefinitivedxRenalTPL AcuteRejection AcuteKidneyInjury INDICATIONSFORRENALREPLACEMENTTHERAPYConsensusgenerallyincludes RefractoryvolumeoverloadSeveremetabolicacidosis HCO3maybevariable butdecliningleveloffactor alsofallingpHto7 1 7 2Hyperkalemia withlevels 6 5 ordocumentedrapidriserefractorytomedicaltherapyMajoruremictargetorganmanifestationsi e pericarditis progressiveneuropathy seizure orunexplainedAMSPlateletdysfunction bleedingdiasthesisAKIinsettingofdialyzabledrug toxin AcuteKidneyInjury INDICATIONSFORRENALREPLACEMENTTHERAPYDespitemodalitiesavailable IHD CRRT mortalityremains50 forAKIincriticallyillpatientsClinicianswillgenerallyoptforRRTinductionpriortodevelopmentoftheabovesymptoms BUNof80 100inabsenceofothersx ssometimesisaindication butpracticesvaryWhileconceptofprophylacticRRThasbeenaroundsince1950 60 s itsbenefitremainsuncertain whetherduetodose timing modalityStudiesbasedonBUNcriteriaStudiesbasedonvolumeremoval ultrafiltrationincardiacpatientsratherthanhigh dosediureticsNobenefitprovenofIHDvsCRRT AKICase 1 45y o malepresentstoERwithsubjectiveweightgain fatigue andvomiting HehadapreviouslynormalPEx serumchemistries3monthspriortocurrentpresentation CurrentlyhehasBP150 110 perorbitaledema LabsincludeBUN85 SCr9 0 UAshows2 protein blood andcellularcastsWhatstatementisleastlikelytobecorrect RenalbiopsyisindicatedPost strepGNisintheDDxExtracapillarycellproliferationislikelySpontaneousresolutionofthisparticularAKIislikelyHigh dosesteroidsareindicated AKICase 2 65y o malepresents7daysfollowingadiagnosticcoronaryangiogram symptomsincludeabdpainandconfusion PExrevealsdiminishedperipheralpuls