急性肾损伤-急性肾功能衰竭

急性肾损伤-急性肾功能衰竭TheEarlyReportofARF“Thediseaseseemsingeneraltocomeonsuddenly.Thepeculiarsymptomisasuddendiminutionofsecretionofurine,whichsoon amountstoacompletesuspensionofit.Theafflictionisprobablyat firstconsideredasretention;butthecatheterbeingemployed,the bladderisfoundtobeempty...afterseveraldays,thepatient beginstotalkincoherently,andshowsatendencytostupor.This increasesgraduallytoperfectcoma,whichinafewdaysmoreis fatal...”JohnAbercombie(1780–1828)sudden(i.e.,hourstodays)reductioninurinevolumeProfileRapid

decreaseinrenalfunctionoverdaystoweeks,causingaaccumulationofnitrogenousproductsintheblood.Oftenresultsfrommajortrauma,illness,orsurgerybutinsomecasesiscausedbyarapidlyprogressive,intrinsicrenaldisease.Symptomsincludeanorexia,nausea,andvomiting,progressingtoseizuresandcomaiftheconditionisuntreated.Fluid,electrolyte,andacid-basedisordersdevelopquickly.Diagnosisisbasedonlaboratorytestsofrenalfunction,includingserumcreatinine,renalfailureindex,andurinarysediment.Othertestsareneededtodeterminethecause.Treatmentisdirectedatthecausebutalsoincludesfluidandelectrolytemanagementandsometimesdialysis.EpidemiologyVariable(inconsistentdefinitions,differentpopulation)

Basedonnewdefinition,AKIoccurs approximately7%inhospitalizedpatientsMortality:VariabledependonetiologyTheModernUnderstandingofARFARFtoAKIDefinitionisbasedonabsoluteincreasein serumcreatinine(Scr)andoliguria

NewconceptsinDefinitionWhat’sthenewdefinition?Earlysingle-centerandmulticenterCohortstudies,administrativedatabasestudiesDefinitionsweredifferent

Houetal.AmJMed74:243–248,1983

NewconceptsinDefinitionTheSecondInternationalConsensusConferenceoftheAcuteDialysisQualityInitiative(ADQI)Group.CritCare.2004;8:R204-R212.DeDecreaseinGFRRIFLEcriteriaNewconceptsinDefinitionAnnewpreciseoperationaldefinitionofAKIisintendedtoemphasizethereversiblenatureofmostrenalinsults.AcuteKidneyInjuryNetwork:reportofaninitiativetoimproveoutcomesinacutekidneyinjury.CritCare.2007;11:R31.AKINcriteriaIn48hoursNewconceptsinDefinition

KDIGOcriteriaNewconceptsinDefinitionNewBiomarkers —CystatinC

—Neutrophilgelatinase–associatedlipocalin(NGAL) —Kidneyinjurymolecule-1

—Interleukin18PathophysiologyEndothelialinjuryfromvascularperturbationsDirecteffectofnephrotoxinsAbolishmentofrenalautoregulationFormationofinflammatorymediatorsPathophysiologyTubularobstruction necrosisandapoptosisoftubularcellsIncreasedtubuloglomerularfeedback elevatedintracellularcalciumlevelsfromtubulardamagecauseaseriesofcellular-levelalterationsEtiologyPre-renal—Underperfusionofkidneysresultsfromvolumedepletion, fluidsequestration,orinadequateperfusionpressures (heartfailure,cirrhosis,orsepsis)— hypoperfusionoffunctioningkidneyleadstoenhanced reabsorptionofNaandwater,resultinginoliguriawith highurineosmolalityandlowurineNa.

Etiology-prerenal Causes examplesECFvolumedepletion excessivediuresis,hemorrhage,GIlosses, transcellularfluid accumulation(ascites, peritonitis,pancreatitis,burns)Lowcardiacoutput cardiomyopathy,MI,cardiactamponade,pulmonaryembolismLowsystemicvascularresistancesepticemia,liverfailure,antihypertensiveagentsIncreasedrenalvascularresistanceliverfailure,NSAIDs,cyclosporine, tacrolimus,anesthesia,renalartery obstruction,renalveinthrombosis,sepsis, hepatorenalsyndromeEtiologyRenal（tubular,interstitial,glomerular,vascular）

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Tubule ATN Ischemia(prolongedorsevereprerenal state) Nephrotoxic

Etiology

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Interstitium Acuteinterstitialnephritis(AIN) -druginduced -certaininfections：pyelonephritis, papillarynecrosis -neoplasticdisorders

Etiology—

Glomerulus

Primary Infectious Rheumatologic Vasculitic

▫antineutrophiliccytoplasmicantibody ▫antinuclearantibodytest ▫antistreptolysinO ▫complementlevels ▫c-reactiveprotein ▫cryoglobulin ▫erythrocytesedimentationrate ▫hepatitispanel(ie,specificallyforhepatitisBandC) ▫renalbiopsyEtiologyPostrenal(10%ofAKI) Urinarytractobstructions(withinoroutside)

stones,tumors,retroperitonealfibrosis

UltrasonographyEtiology-postrenal Causes Examples Tubularprecipitation uricacid(tumorlysis),sulfonamides,, acyclovir,methotrecxate,Caoxalate (ethyleneglycolingestion),myeloma protein,myoglobin Ureteralobstruction Intrinsic:calculi,clots,slougher renaltissue, fungusball,edema,malignancy, congenitaldefects

Extrinsic:malignancy,retroperitonealfibrosis, ureteraltraumaduringsurgeryorhigh impactinjury Bladderobstruction Mechanical:prostatichypertrophyorcancer, bladdercancer,urethralstrictures, phimosis,urethralvalves,obstructed indwellingurinarycatheter

Neurogenic:anticholinergics,upperorlower motorneuronlesionSymptomsandsigns

Oftheunderlyingillnessorsurgicalprocedurethatprecipitatedrenaldeterioration.Uremiasymptoms:anorexia,nausea,vomiting,weakness,myoclonicjerks,seizures,confusionandcoma.PE:edema,palpablebladderetc.DiagnosisSuspectedwhenurineoutputfallsorserumBUNandScrriseSeekanunderlyingcauseLaboratorytests: CBC,BUN/Scr,electrolytes,urinetestsandotherneededbycausedeterminationDiagnosticEvaluation Index Prerenal Postrenal ATN AGN U/Posmolality >1.5 1~1.5 1~1.5 1~1.5 UrineNa(mmol/L) <20 >40 >40 <30 Fractionalexcretion ofNa(FENa) <0.01 >0.04 >0.02 <0.01 Renalfailureindex <1 >2 >2<1AdaptedfromMillerTR,etal:urinarydiagnosticindicesinacuterenalfailure.U/P:urine/plasmaRenalfailureindex:U/PNa+U/PcreatinineSpecialScenariosContrast-inducednephropathy(CIN) —increaseinserumcreatininelevelsthatis 25%orhigher(0.5mg/dL)within72hoursofcontrastmediaadministration —riskfactorsforCINincludeolderage,diabetes, underlyingchronicCKD,multiplemyeloma,andvolumedepletion. —Vasomotoralterations,freeradicalformation—prehydration,temporarydiscontinuationofACE inhibitors,angiotensinreceptorblockers,anddiureticsSpecialScenariosSepsis —19%inmoderatesepsis,23%inseveresepsis,and51%insepticshock —AKI+sepsis:70%mortalityrateversus45%amongpatientswithAKIalone —nitricoxidesynthases,cytokines,chemokines, andadhesionmolecules —earlygoal-directedtherapy,hemodialysisTreatmentVariedanddependonetiologicfactorsPrerenalazotemiafromvolumedepletionisusuallyresponsivetoisotonicsalinerepletionATNrequiresthediscontinuationofnephrotoxicagents,maintenanceofoptimumhemodynamics,andclosesurveillanceforcomplicationsofrenaldysfunction(eg,acidosis,electrolyteabnormalities)PostrenaletiologiesdictateobstructionremovalTreatmentEmergencytreatment—Life-threateningcomplications Pulmonaryedema: O2,IVvasodilators Hyperkalemia: IVinfusionof10%Ca gluconate10ml, dextrose50g,insulin5~10units. Severeacidosis(pH<7.2) IVNaHCO3(<150mEqin1Lof5%D/W)TreatmentFluidcontrolDailywaterintake=sensibledehydrationvolume(previous24hours)+insensibledehydration–endogenicwater(1gprotein:0.4ml;lipid:1ml;glucose:0.6ml)[insensibledehydration–endogenicwater]≈500~1000ml/dTreatmentNumerouspharmacologicagents:insulin-likegrowthfactor1,thyroxine,atrialnatriureticpeptide,dopamine,andloopdiuretics,effectiveinpreventingoramelioratingexperimentalAKI.noneofthesesubstanceshasbeentranslatedsuccessfullytoclinicalpractice.clinicalmanagementofAKIisprimarilysupportive

Treatment:NutritionalsupportNUTRITIONALSTATUSINAKI —PatientswithAKIintheICU,evenmorethanothercriticallyillpatients,areatriskofnutritionaldepletion —evaluationinthisclinicalconditionisdifficultasmostof thecommonlyutilizedtraditionalnutritionaltoolsareoftenmisleading —protein-energywasting(PEW)aconditionofdecreasedbodystoresof proteinandenergyfuelstores(i.e.,leanbodymassandfatmasses)

biochemical(suchasalbuminorprealbumin), bodyweightloss,decreasedmusclemasslowenergyandproteinintakesInternationalSocietyofRenalNutritionandMetabolism(ISRNM)Treatment:NutritionalsupportAKIisassociatedwithalterationsofwater,electrolyteandacid-basemetabolism,andalsowithspecificchangesinprotein,carbohydrateandlipidmetabolism —hyperglycemiaandinsulinresistance —proteolysisofskeletalmuscleproteinswithincreasedaminoacidturnoverandnegativenitrogenbalance —alteredlipidmetabolism TG,VLDL↑TC,HDL,LDL↓Treatment:NutritionalsupportNUTRIENTREQUIREMENTSINAKI Macronutrients—dependsmoreontheseverityofunderlyingdisease,preexistingnutritionalstatusandacute/chroniccomorbidities,thanonAKIitselfTreatment:NutritionalsupportGOALSOFNUTRITIONALSUPPORTINAKI—ensurethedeliveryofenergyandproteininsuchamountsastopreventprotein-energywasting—preserveleanbodymassandnutritionalstatus—avoidfurthermetabolicderangementsandcomplications—improvewoundhealing—supportimmunefunctionandtoreducemortalityTreatment:replacementtherapyRRTisthecentralcomponentofcareforpatientswithsevereAKI. generallyacceptedindicationsforRRTincludevolumeoverload,hyperkalemia,metabolicacidosis,andoverturemicsymptomsTreatment:replacementtherapyFordecades,continuousre