腎內科全套課件

IgAnephropathy

IgANephropathy:Berger’sDiseasethemostcommonlesionfoundtocauseprimaryglomerulonephritispeakincidenceinthesecondandthirddecadesoflife2:1maletofemalegreatestfrequencyinAsiansandCaucasiansrelativelyrareinblacksIgANephropathylargeundiagnosed"latent"IgAnephropathyinthegeneralpopulationtheprocessofmesangialIgAdepositionislikelytobeseparatefromtheinductionofglomerularinjuryIgAdepositiondoesnotnecessarilyneedtobefollowedbynephritisIgADepositionisCommonIgAdepositioninotherformsofglomerulonephritisthinbasementmembranenephropathylupusnephritisminimalchangediseasediabeticnephropathyIgANephropathyManypatientsaredetectedonroutineurinescreeningasymptomatichematuriaand/orproteinuriahigherprevalenceactiveurinetestingprogramlowthresholdforrenalbiopsyIgANephropathyIgAnephropathyisestablishedonlybykidneybiopsyImmunofluorescencemicroscopydemonstratinglarge,globularmesangialIgAdepositsIgAoftenaccompaniedbyC3andIgGinthemesangiumIgANephropathyEMelectrondensedepositsthatarelimitedtothemesangialregionsIgANephropathymesangialglomerulonephritisshowingsegmentalareasofincreasedmesangialmatrixandcellularityConditionsassociatedwithIgAnephropathyIdiopathic(mostcases)HepaticcirrhosisGlutenenteropathyHIVinfectionMinimalchangediseaseMembranousGNWegener’sgranulomatosisankylosingspondylitisSmallcellcarcinomaDisseminatedtuberculosisIgANephropathyInitiatingeventinthepathogenesisisthemesangialdepositionofIgACodepositsofIgGandcomplementcommonlyseenmaycontributetodiseaseseverityBetweenepisodesofgrosshematuriapersistentmicrohematuria,proteinuria,orboth.Grosshematuriahasalsofollowedtonsillectomy,vaccinations,strenuousphysicalexercise,andtrauma.

IncreasedPlasmaIgALevelsNotaloneissufficienttoproducemesangialIgAdepositsFoundin50%ofcasesIgAisprobablyaccumulatedanddepositedbecauseofasystemicabnormalityratherthanadefectintrinsictothekidneyIgANephropathyTwocommonpresentationsepisodicgrosshematuria40-50%upperrespiratorytractinfection,or,lessoften,gastroenteritispersistentmicroscopichematuria30-40%asymptomatic,witherythrocytes(RBCs),RBCcasts,andproteinuriadiscoveredonurinalysisIgANephropathyNephroticrangeproteinuriaisuncommonoccurringinonly5%ofpatientsIndicatesmoreadvanceddiseaseApproximately1-2%ofallpatientswithIgAnephropathydevelopESRDeachyearHypertensionseldomoccursatthetimeofinitialpresentationMorbidityandMortalityfollowabenigncourseinmostcasesatriskforslowprogressiontoESRDapproximately15%ofpatientsby10years20%by20yearsIgANephropathyOutcomes20-30%progresstoESRDover20years1-2%peryearClinicalpredictorsofpoorrenaloutcomeAbsenceofgrosshematuriaMaleOlderonsetageHeavyproteinuriaElevatedCr>2-2.5IgANephropathyOutcomesTherapyremainstobedefinedAntibioticsTonsillectomyCyclophosphamide,dipyridamoleHighdoseimmunoglobulintherapyStatinsFishOilsAceinhibitionCellcept(mycophenolatemofetil)IgANephropathyOutcomesAceinhibitorsEffectivelyreduceproteinuriaACE-IpreserveGFRinIgAQuestionableaddititiveeffectwithARBSIgANephropathyOutcomesFishOilMetaanalysisconcludedtheremaybeaminorbenefitinheavyproteinuriaDillon1997JASNLowdoesomega3fattyacidsaseffectiveashighdoseCellceptEstablishedusefortransplantNotthatmuchimprovementforIgAIgATreatmentSummaryIfUprot<0.5g/dandCrCl>70ObserveandconsiderACEIorARBIfUprot>0.5g/dandCrCl>70ACEI/ARBfortargetbp125/75IfUprot1-3g/dwithCrCl>70MaximalACEI/ARBConsider6monthsofhighdosesteroidsandtaperfor6moIfUprot>3g/dandCrCl<70ordecliningSteroidsplusCytotoxicsPossiblemaintenancewithAZAorMMFTransplantRecipientshighrecurrencerateinrenaltransplantrecipientswhohaveIgAnephropathy25-60%disappearanceofthedepositsfromdonorkidneyswithIgAnephropathywhentransplantedintodonorswithoutthediseaseCasePresentation44-year-oldwhitemalewithcomplaintsofhematuriahadassociatedabdominalpainnohistoryofknownCKDandhasnotactuallyseenadoctorin25yearsnohistoryofotherhematuria,prostatetrouble,dysuria,nocturia,incontinencenotonanyoutpatientanticoagulation20yearsoftobaccoabuseCasePresentationrecentupperrespiratory

infection2weeksagowithfeversandchillsfoamyurinedeniesanyrecentknownUTI,over-the-counterNSAIDs,history

ofnephrolithiasis,contrastedprocedure,physicalexerciseCasePresentationPositivesigns:RecentURItwoweeksago10poundweightgainwithedemaHematuriaFoamyurineAbdominalpainCasePresentation:LabCa9.6Alb1.65222.0NoPhosorMgUAiscloudywith

positivenitrite,10gramsprotein,toonumeroustocountredcells,tracebacteria,1-5whitecells

CasePresentation:LabsCToftheabdomenandpelviswasnegative

foranystone,multipleloopsoffluid-fillednondilatedsmallbowelwithoutobstructionorcontractedGBCasePresentation:LabsAllnegativeComplementsANA,dsDNAHepatitisprofileAntiGBMPandCANCA’sHIVASODifferentialDiagnosisBacktoourcase44yowithhematura,proteinuria,andlowerextremityedematwoweeksafteranURINopreviousknowCKDorAKICrnow2.0mg/dl10gramsproteinuriaHyperlipidemiaRedBloodCellCastsGlomerularhematuriaDysmorphicrbc’sglomerulardamageruleouturologiccausesDifferentialDiagnosis:GlomerulonephritisPostinfectiousGNIgAnephropathyThinbasementmembraneMesangialproliferativeGNSLEGoodpasture’ssyndromeVasculitisCryoglobulinemiaHIVMembranoproliferativeglomerulonephritisRapidlyprogressiveGNFocalglomerulosclerosisMembranousnephropathyAmyloidosisMultipleMyelomaDMHUSRenalBiopsy:IgANephropathyLightmicroscopy-MesangialhypercellularityIgAispredominantlypolymericIgA1mainlyderivedfromthemucosalimmunesystem

PatientProgressionCrcontinuedtoworsenwithdiseaseprogressionMarchCr:2.0AprilCr:3.09–4.2InitiationofCytoxanandSteroids(2cycles)ACEIcausedhyperkalemiaFishOil,BB,Lasix,Zaroxolyn,Statin,PPI,OscalMayCr:5.2June18th:8.76ESRDwithhemodialysisinitiationUncontrollableedemaandpulmonaryedemadespitediureticsQuestion1WhichofthefollowingisthemostpredictiveforprogressionofIgAA-elevatedlevelsofIgAB-elevatedCratbaselinediagnosisC-malegenderD-absenceofgrosshematuriaQuestion1WhichofthefollowingisthemostpredictiveforprogressionofIgAA-elevatedlevelsofIgAB-elevatedCratbaselinediagnosisC-malegenderD-absenceofgrosshematuriaQuestion2Youareseeinga30yrAsianwomanwithprovenIgA.HerUproteinis3.5g/ddespitemaximalACEI,Bpis100/70,Crstableat1.6forthepastyear.DiffusefootprocesseffacementisseenonEM.Whatisthenextstepformanagement?A-AddARBB-AddMMFC-AddsteroidsD-AddfishoilsE-TonsillectomyA35yearoldwoman,anursinghomeassistant,presentswithchronicacidosisthatisdifficulttomanage.LabevaluationshowedNa143,K2.8Cl118,HCO315BUN18,Cr0.7.ABGrevealsph7.38Pco231,Pao2100.U/Aresultswerenormalwithurinephof5.0.UrineNawas40K5andUrineCl150.Whichdisorderbestcharacterizesthisptssyndrome.DiureticabuseLaxativeabuseDistalrenaltubularacidosisProximalrenaltubularacidosisType4renaltubularacidosisOUTLINERenaltubularacidosis(RTA)isappliedtoagroupoftransportdefectsinthereabsorptionofbicarbonate(HCO3-),theexcretionofhydrogenion(H+),orboth.TheRTAsyndromesarecharacterizedbyarelativelynormalGFRandametabolicacidosisaccompaniedbyhyperchloremiaandanormalplasmaaniongap.OBJECTIVESPhysiologyofRenalacidification.TypesofRTAandcharacteristicsLabdiagnosisofRTAApproachtoapatientwithRTATreatmentPhysiologyofRenalAcidificationKidneysexcrete50-100meq/dayofnoncarbonicacidgenerateddaily.ThisisachievedbyH+secretionatdifferentlevelsinthenephron.ThedailyacidloadcannotbeexcretedasfreeH+ions.SecretedH+ionsareexcretedbybindingtoeitherbuffers,suchasHPO42-andcreatinine,ortoNH3toformNH4+.TheextracellularpHistheprimaryphysiologicregulatorofnetacidexcretion.

Renalacid-basehomeostasismaybebroadlydividedinto2processesProximaltubularabsorptionofHCO3-(Proximalacidification)DistalUrinaryacidification.ReabsorptionofremainingHCO3-thatescapesproximally.Excretionoffixedacidsthroughbuffering&AmmoniarecyclingandexcretionofNH4+.ProximaltubulephysiologyProximaltubulecontributestorenalacidificationbyH+secretionintothetubularlumenthroughNHE3transporterandbyHCO3-reabsorption.Approx.85%offilteredHCO3-isabsorbedbytheproximaltubule.Theremaining15%ofthefilteredHCO3-isreabsorbedinthethickascendinglimbandintheoutermedullarycollectingtubule.ProximaltubulephysiologyMultiplefactorsareofprimaryimportanceinnormalbicarbonatereabsorptionThesodium-hydrogenexchangerintheluminalmembrane(NHE3).TheNa-K-ATPasepumpTheenzymecarbonicanhydraseII&IVTheelectrogenicsodium-bicarbonatecotransporter(NBC-1)..AmmoniarecyclingAmmoniumsynthesisandexcretionisoneofthemostimportantwayskidneyseliminatenonvolatileacids.Ammoniumisproducedviacatabolismofglutamineintheproximaltubulecells.LuminalNH4+ispartiallyreabsorbedinthethickascendinglimbandtheNH3thenrecycledwithintherenalmedullaAmmoniaRecyclingThemedullaryinterstitialNH3reacheshighconcentrationsthatallowNH3todiffuseintothetubularlumeninthemedullarycollectingtubule,whereitistrappedasNH4+bysecretedH+.DistalUrinaryAcidificationThethickascendinglimbofHenle’sloopreabsorbsabout15%ofthefilteredHCO3-loadbyamechanismsimilartothatpresentintheproximaltubule,i.e.,throughNa+-H+apicalexchange(NHE3).H+secretionThecollectingtubule(CT)isthemajorsiteofH+secretionandismadeupofthemedullarycollectingduct(MCT)andthecorticalcollectingduct(CCT).AlphaandBeta-intercalatedcellsmakeup40%oftheliningwhilePrincipalcellsandcollectingtubulecellsmakeuptheremainder.Alpha-IntercalatedCellsarethoughttobethemaincellsinvolvedwithH+secretionintheCT.ThisisaccomplishedbyanapicallyplacedH+-K+-ATPaseandH+-ATPasewithabasolateralCl-/HCO3-exchangerandtheusualbasolateralNa+-K+ATPase.Beta-IntercalatedCellsincontrasttotheabovehavealuminalCl-/HCO3-exchangerandabasolateralH+-ATPase.TheyplayaroleinbicarbonatesecretionintothelumenthatislaterreabsorbedbytheCAIVrichluminalmembraneofmedullarycollectingduct.CCTH+secretionisindividuallycoupledtoNa+transport.ActiveNa+reabsorptiongeneratesanegativelumenpotentialfavoringsecretionofH+andK+ions.IncontrasttheMCTsecretesH+ionsindependentlyofNa+.MedullaryportionoftheCollectingductisthemostimportantsiteofurinaryacidificationPrincipalcellsAldosteroneandRenalacidificationFavorsH+andK+secretionthroughenhancedsodiumtransport.Recruitsmoreamiloridesensitivesodiumchannelsintheluminalmembraneofthecollectingtubule.EnhancesH+-ATPaseactivityincorticalandmedullarycollectingtubules.AldosteronealsohasaneffectonNH4+excretionbyincreasingNH3synthesisSummaryH+secretion,bicarbonatereabsorptionandNH4+productionoccurattheproximaltubule.LuminalCAIVispresentintheluminalmembraneatthissiteandinMCT.NH4+reabsorptionoccursatTALofloopofHenleandhelpsinammoniarecyclingthatfacilitatesNH4+excretionatMCT.H+secretionoccursintheCCTeitherdependentorindependentofNaavailabilityandintheMCTasanindependentprocess..OBJECTIVESPhysiologyofRenalAcidification.TypesofRTAandcharacteristicsLabdiagnosisofRTAApproachtoapatientwithRTATreatmentTYPESOFRTA

ProximalRTA(type2)IsolatedbicarbonatedefectFanconisyndrome

DistalRTA(type1)ClassictypeHyperkalemicdistalRTAHyperkalemicRTA(Type4)

PROXIMALRTAProximalRTA(pRTA)isadisorderleadingtoHCMAsecondarytoimpairedproximalreabsorptionoffilteredbicarbonate.Sincetheproximaltubuleisresponsibleforthereabsorptionof85-90%offilteredHCO3-adefectatthissiteleadstodeliveryoflargeamountsofbicarbonatetothedistaltubule.

Thisleadstobicarbonaturia,kaliuresisandsodiumlosses.ThuspatientswillgenerallypresentwithhypokalemiaandaHCMA..IsolateddefectsinPCTfunctionarerarelyfound.MostpatientswithapRTAwillhavemultipledefectsinPCTfunctionwithsubsequentFanconiSyndrome.ThemostcommoncausesofFanconisyndromeinadultsaremultiplemyelomaanduseofacetazolamide.Inchildren,cystinosisisthemostcommon.pRTAisaselflimitingdisorderandfallofserumHCO3_below12meq/lisunusual,asthedistalacidificationmechanismsareintact..Urinephbecomeremainsacidic(<5.5)mostlybutbecomesalkalinewhenbicarbonatelossesarecorrected.FEHCO3increases(>15%)withadministrationofalkaliforcorrectionofacidosisCauseofhyokalemiainType2RTAMetabolicacidosisinandofitselfdecreasespRTNa+reabsorptionleadingtoincreaseddistaltubuledeliveryofNa+whichpromotesK+secretion.ThepRTAdefectalmostinevitablyleadstosaltwasting,volumedepletionandsecondaryhyperaldosteronism.Therateofkaliuresisisproportionaltodistalbicarbonatedelivery.Becauseofthisalkalitherapytendstoexaggeratethehypokalemia.PatientswithpRTArarelydevelopnehrosclerosisornephrolithiasis.Thisisthoughttobesecondarytohighcitrateexcretion.Inchildren,thehypocalcemiaaswellastheHCMAwillleadtogrowthretardation,rickets,osteomalaciaandanabnormalvitaminDmetabolism.Inadultsosteopeniaisgenerallyseen.DISTALRTADistalRTA(dRTA)isadisorderleadingtoHCMAsecondarytoimpaireddistalH+secretion.Itischaracterizedbyinabilitytolowerurinephmaximally(<5.5)underthestimulusofsystemicacidemia.TheserumHCO3-levelsareverylow<12meq/l.Itisoftenassociatedwithhypercalciuria,hypocitraturia,nephrocalcinosis,andosteomalacia.ThetermincompletedistalRTAhasbeenproposedtodescribepatientswithnephrolithiasisbutwithoutmetabolicacidosis.Hypocitraturiaistheusualunderlyingcause.Themostcommoncausesinadultsareautoimmunedisorders,suchasSj?gren'ssyndrome,andotherconditionsassociatedwithchronichyperglobulinemia.Inchildren,type1RTAismostoftenaprimary,hereditarycondition.SecretorydefectscausingDistalRTANonsecretorydefectscausingDistalRTAGradientdefect:backleakofsecretdH+ions.Ex.AmphotericinBVoltagedependentdefect:impaireddistalsodiumtransportex.Obstructiveuropathy,sicklecelldisease,CAH,Lithiumandamilorideetc.ThisformofdistalRTAisassociatedwithhyperkalemia(HyperkalemicdistalRTA)AhighurinarypH(5.5)isfoundinthemajorityofpatientswithasecretorydRTA.ExcretionofammoniumislowasaresultoflessNH4+trapping.Thisleadstoapositiveurineaniongap.UrinePCO2doesnotincreasenormallyafterabicarbonateloadreflectingdecreaseddistalhydrogenionsecretion.Serumpotassiumisreducedin50%ofpatients.ThisisthoughttobefromincreasedkaliuresistooffsetdecreasedH+andH-K-ATPaseactivity.Type4RTA(HyperkalemicRTA)ThisdisorderischaracterizedbymodestHCMAwithnormalAGandassociationwithhyperkalemia.Thisconditionoccursprimarilyduetodecreasedurinaryammoniumexcretion.Hypoaldosteronismisconsideredtobethemostcommonetiology.OthercausesincludeNSAIDS,ACEinhibitors,adrenalinsufficiencyetc.MechanismofactionIncontrasttohyperakalemicdistalRTA,theabilitytolowerurinephinresponsetosystemicacidosisismaintained.Nephrocalcinosisisabsentinthisdisorder.OBJECTIVESPhysiologyofRenalAcidification.TypesofRTAandcharacteristicsLabdiagnosisofRTAApproachtoapatientwithRTATreatmentLabdiagnosisofRTARTAshouldbesuspectedwhenmetabolicacidosisisaccompaniedbyhyperchloremiaandanormalplasmaaniongap(Na+-[Cl-+HCO3-]=8to16mmol/L)inapatientwithoutevidenceofgastrointestinalHCO3-lossesandwhoisnottakingacetazolamideoringestingexogenousacid.FunctionalevaluationofproximalbicarbonateabsorptionFractionalexcretionofbicarbonateUrinephmonitoringduringIVadministrationofsodiumbicarbonate.FEHCO3isincreasedinproximalRTA>15%andislowinotherformsofRTA.FunctionalEvaluationofDistalUrinaryAcidificationandPotassiumSecretion

UrinephUrineaniongapUrineosmolalgapUrinePco2TTKGUrinarycitrateUrinephInhumans,theminimumurinepHthatcanbeachievedis4.5to5.0.Ideallyurinephshouldbemeasuredinafreshmorningurinesample.Alowurinephdoesnotensurenormaldistalacidificationandviceversa.TheurinepHmustalwaysbeevaluatedinconjunctionwiththeurinaryNH4+contenttoassessthedistalacidificationprocessadequately.Urinesodiumshouldbeknownandurineshouldnotbeinfected.UrineAnionGapUrineAG=Urine(Na+K-Cl).TheurineAGhasanegativevalueinmostpatientswithanormalAGmetabolicacidosis.Patientswithrenalfailure,type1(distal)renaltubularacidosis(RTA),orhypoaldosteronism(type4RTA)areunabletoexcreteammoniumnormally.Asaresult,theurineAGwillhaveapositivevalue.Thereare,however,twosettingsinwhichtheurineAGcannotbeused.Whenthepatientisvolumedepletedwithaurinesodiumconcentrationbelow25meq/L.WhenthereisincreasedexcretionofunmeasuredanionsUrineosmolalgapWhentheurineAGispositiveanditisunclearwhetherincreasedexcretionofunmeasuredanionsisresponsible,theurineammoniumconcentrationcanbeestimatedfromcalculationoftheurineosmolalgap.UOG=Uosm-2x([Na+K])+[ureanitrogen]/2.8+[glucose]/18.UOGof>100representsintactNH4secretion.UrinePco2Measureofdistalacidsecretion.InpRTA,unabsorbedHCO3reactswithsecretedH+ionstoformH2CO3thatdissociateslowlytoformCO2inMCT.Urine-to-bloodpCO2is<20inpRTA.Urine-to-bloodpCO2is>20indistalRTAreflectingimpairedammoniumsecretion.TTKGTTKGisaconcentrationgradientbetweenthetubularfluidattheendofthecorticalcollectingtubuleandtheplasma.TTKG

=

[UrineK

÷

(Urineosmolality/Plasmaosmolality)]

÷

PlasmaK.Normalvalueis8andabove.Value<7inahyperkalemicpatientindicateshypoaldosteronism.Thisformulaisrelativelyaccurateaslongastheurineosmolalityexceedsthatoftheplasmaurinesodiumconcentrationisabove25meq/LUrinecitrateTheproximaltubulereabsorbsmost(70-90%)ofthefilteredcitrate.Acid-basestatusplaysthemostsignificantroleincitrateexcretion.Alkalosisenhancescitrateexcretion,whileacidosisdecreasesit.Citrateexcretionisimpairedbyacidosis,hypokalemia,high–animalproteindietandUTI.OBJECTIVESPhysiologyofRenalacidification.TypesofRTAandcharacteristicsLabdiagnosisofRTAApproachtoapatientwithRTATreatmentOBJECTIVESPhysiologyofRenalacidification.TypesofRTAandcharacteristicsLabdiagnosisofRTAApproachtoapatientwithRTATreatmentTreatmentProximalRTAAmixtureofNa+andK+salts,preferablycitrate,ispreferable.10to15meqofalkali/kgmayberequiredperdaytostayaheadofurinarylosses.Thiazidediureticmaybebeneficialiflargedosesofalkaliareineffectiveornotwelltolerated.

DistalRTABicarbonatewastingisnegligibleinadultswhocangenerallybetreatedwith1to2meq/kgofsodiumcitrate(Bicitra)orbicarbonate.Potassiumcitrate,aloneorwithsodiumcitrate(Polycitra),isindicatedforpersistenthypokalemiaorforcalciumstonedisease.ForpatientswithhyperkalemicdistalRTA,high-sodium,low-potassiumdietplusathiazideorloopdiureticifnecessary.IntroductionUTIsrepresentawidevarietyofsyndromesincludingurethritis,cystitis,prostatitis,andpyelonephritis.Oneofthemostcommonlyoccurringinfections.IntroductionYoungwomenareparticularlysusceptible,40%ofallwomenwillsufferatleastoneUTIatsomepoint.Infectioninmenoccurslessfrequentlyuntiltheageof50,whenincidenceinmenandwomenissimilar.DefinitionItisthepresenceofmicroorganismsintheurinarytractthatcannotbeaccountedforbycontamination.TheorganismshavethepotentialtoinvadethetissuesoftheUTandadjacentstructures.DefinitionAUTIcanmanifestasseveralsyndromesassociatedwithaninflammatoryresponsetomicrobialinvasionthatrangefromasymptomaticbacteriuriatopyelonephritis.ClassificationAccordingtoanatomicsiteofinvolvement:Lowertractinfection:cystitis,urethritis,prostatitisUppertractinfection:pyelonephritis,involvingthekidneysClassificationAccordingtoDegree1-UncomplicatedOccurinindividualswholackstructuralorfunctionalabnormalitiesintheUTthatinterferewiththenormalflowofurine.MostlyinhealthyfemalesofchildbearingageClassificationAccordingtoDegree2-ComplicatedpredisposinglesionoftheUTsuchascongenitalabnormalityordistortionoftheUT,astoneacatheter,prostatichypertrophy,obstruction,orneurologicaldeficitAllcaninterferewiththenormalflowofurineandurinarytractdefenses.RecurrentUTIsMultiplesymptomaticinfectionswithasymptomaticperiodsReinfection:causedbyadifferentorganismthanoriginallyisolatedandaccountforthemajorityofrecurrentUTIs.Relapse:repeatedinfectionswiththesameinitialorganismandusuallyindicateapersistentinfectioussource.OtherDefinitionsAsymptomaticbacteriuriaCommonamongtheelderlyBacteriuria>105bacteria/mlofurinewithoutsymptomsSymptomaticabacteriuria:SymptomsoffrequencyanddysuriaintheabsenceofsignificantbacteriuriaOtherDefinitionsSignificantbacteriuriaMorethan105bacteria/ml(CFU)ofurineincleancatchspecimen1/3ofsymptomaticwomenhaveCFUcountsbelowthislevelAbacterialcountof100CFU/mlhasahighpositivepredictivevalueofcystitisinsymptomaticwomenOtherDefinitionsCountlessthan105mayrepresenttrueinfectionincertainsituationsConcurrentantibacterialdrugadministrationRapidurineflowLowurinePHUppertractobstructionEtiologyThemicroorganismthatcauseUTIsusuallyoriginatefromthebowelfloraofthehostUncomplicatedUTI:

E.coliaccountsfor85%S.saprophyticus5-15%K.pneumoniae,Pseudomonas,andEnterococcus5-10%S.epidermidisifisolatedshouldbeconsideredacontaminationEtiologyComplicatedUTIsOccursbecauseofanatomic,functional,orpharmacologicalfactorsthatpredisposesthepatienttopersistentinfection,recurrentinfection,ortreatmentfailure.EtiologyComplicatedUTIsMorevariedandgenerallymoreresistantE.coli50%K.pneumoniae,Pseudomonas,Enterococcus,spEtiologyComplicatedUTIsEnterococcusfecalis2ndmostfrequentlyisolatedorganisminhospitalizedpatientsSPinfectionismorecommonlyaresultofbacteremiaproducingmetastaticabscessesinthekidneyCandidaiscommoncauseofUTIincriticallyillandchronicallycatheterizedpatientsEtiologyThemajorityofUTIsarecausedbyasingleorganismInpatientswithstones,indwellingcatheter,orchronicrenalabscessesmultipleorganismsmaybeisolatedAlthoughthismaybeduetocontaminationandarepeatevaluationshouldbedone.PredisposingfactorsAbnormalitiesintheUTthatinterferewithnaturaldefenses1-Obstructioncaninhibiturineflow,disruptingthenaturalflushingandvoidingeffectinremovingbacteriafromthebladderandresultinginincompleteemptyingPredisposingfactorsAbnormalitiesintheUTthatinterferewithnaturaldefenses.2-Conditionthatresultinresidualurinevolumese.g.prostatichypertrophy,urethralstricture,calculi,tumors,anddrugsuchasanticholinergicagents,neurologicalmalfunctionsassociatedwithstroke,diabetes,andspinalcordinjuries.PredisposingfactorsAbnormalitiesintheUTthatinterferewithnaturaldefenses.3-Otherriskfactorsinclude:urinarycatheter,mechanicalinstrumentation,pregnancy,andtheuseofspermicidiesanddiaphragmsClinicalpresentationsLowertractinfection:

Includedysuria,urgency,frequency,nocturia,suprapubicheaviness,andhematuriainwomen.NosystemicsymptomsUppertractinfection:Flankpain,costovertebraltenderness,abdominalpain,fever,nausea,vomitingandmalaise.ClinicalpresentationsElderlypatients:FrequentlydoexperiencespecificurinarysymptomsAlteredmentalstatus,changeeatinghabits,orGIsymptomsPatientswithcathetersWillhavenolowertractsymptomsJustflankpainandfeverClinicalpresentationsAcutebacterialprostatitisPerineal,sacral,orsuprapubicpainFever,urinaryretention,Frequency,urgency,nocturiaswollen,tender,warm,andinduratedprostateClinicalpresentationsChronicbacterialprostatitisVaguevoidingdifficultiesLowerbackpainPerinealandsuperapubicdiscomfortManypatientsareasymptomaticPhysicalexaminationoftheprostateisunremarkableLaboratoryfindingsSymptomsaloneareunreliablefordiagnosisExaminationoftheurineisthecornerstoneofdiagnosisCollectionofurine:MidstreamcleancatchmethodispreferredmethodLaboratoryfindingsCollectionofurine:Catheterizationforpatientwhoareuncooperativeorunabletovoid,butintroductionofbacteriainthebladderoccursat1-2%Suprapubicaspirationbypassesthecontaminatingorganismintheurethra,safeandpainless.Diagnosis:BasedonisolationofsignificantnumbersofbacteriafromaurinespecimenMicroscopicexamination

isperformedbypreparingagramstainthatindicatesthemorphologyoftheorganismandhelpdirecttheselectionofanappropriateAB.Diagnosis:Microscopicexamination

Thepresenceofoneorganismperoil-immersionfieldinanuncentrifugedsamplecorrelateswith100,000bacteria/mlDiagnosis:Hematuria,non-specific,mayindicateotherdisorderssuchascalculiortumorProtenuriaisfoundinthepresenceofinfec