9泌尿系統(tǒng)病理學(xué)課件1

Diseasesofurinarysystemandmalegenitalsystem

徐緩DepartmentofPathologyWestChinahospital2014.10DiseasesofurinarysystemandNephrologyUrologyNephrologyOutlineGlomerulonephritis(GN)TubulointerstitialnephritisUrinaryoutflowobstructionTumorsofurinarysystemProstateDisease,TestisandPenisTumorOutlineGlomerulonephritis(GN)Theincidencerateofchronickidneydisease(CKD)is9.4%to11.8%inChina,thereisonepatientforeverytenpeopleTheoccurrenceisoccult,20%ofthepatientsatdiagnosisareonlatestageThesecondThursdayofMarchisdeclaredastheWorldKidneyDay(WKD).March13,2014isthe9thWKD.ThetopicforWKD2014is“CKDinolderpeople”TheincidencerateofchronicCTscan12CTscan12GrossviewGrossviewFunctionsofthekidneyExcretionmetabolicwasteproductsRegulatingfluidandelectrolytebalanceInfluencingacid-basebalanceSecretinghormones(renin,erythropoietin,et.al)FunctionsofthekidneyExcretiNormalnephronNormalnephronFilteringmembraneFilteringmembrane9泌尿系統(tǒng)病理學(xué)課件1FilteringmembraneAthinlayeroffenestratedendothelial(Fenestra,70to100nmindiameter)Theglomerularbasementmembrane(GBM)Thefootprocessesofvisceralepithelialcell(slitdiaphragm)FilteringmembraneAthinlayerFunctionof

filteringmembraneHighpermeabilitytowaterandsmallsoluteGlomurularbarrierfunction

Size-dependentbarrierfunctionCharge-dependentbarrierfunctionFunctionof

filteringmembrOutlineGlomerulonephritis(GN)TubulointerstitialnephritisUrinaryoutflowobstructionTumorsofurinarysystemProstateDisease,TestisandPenisTumorOutlineGlomerulonephritis(GN)EtiologyofglomerulardiseasesPrimary(majority):diseaseprocessappearstostartwithintheglomerulusSecondary:diseaseprocessissecondarytosystemicdisease(SLE,vasculardiseases,diabetesmellitus,amyloidosis)Hereditary:congenitaldiseases(Alportsyndrome,Fabry’sdisease)EtiologyofglomerulardiseasePrimaryglomerulonephritiskidneyistheonlyorpredominantorgan

involvedPrimaryglomerulonephritiskidnEtiologyandPathogenesis

ImmunemechanismsunderliethemajorityofprimaryGN.Themostcommonmechanismisantibody-medicatedinjury.Twobasicformsofantibody-associatedinjury:Injuryresultingfromdepositionofsolublecirculatingantigen-antibodycomplexesintheglomeruliInjurybyantibodiesreactinginsituwithintheglomeruliEtiologyandPathogenesisImmuCirculatingImmuneComplexNephritisCausedbythetrappingofcirculatingantigen-antibodycomplexeswithinglomeruliTheantibodieshavenoimmunologicspecificityforglomerularconstituentsTypeⅢhypersensitivityreactionTheantigensmaybeofendogenousorexogenousoriginsCirculatingImmuneComplexNepCirculatingImmuneComplexNephritisTheelectron-densedepositslieinthemesangium,betweentheendothelialcellsandtheGBM(subendothelialdeposits)orbetweentheGBMandthepodocytes(subepithelialdeposits)ThedepositsmaybedegradedbymonocytesandmesangialcellsCirculatingImmuneComplexNepInSituImmuneComplexDepositionAntibodiesreactdirectlywithintrinsictissueantigen,orantigens“planted”intheglomerulifromthecirculation.AutoantibodiesagainstcomponentsoftheGBMarethecauseofanti-GBM–mediateddisease,oftenassociatedwithsevereinjury.Thepatternofdepositionislinear.AntibodiesmayalsobeformedagainstantigensthatareplantedintheGBM.Theresultantinsituimmunecomplexesmayshowagranularpatternofdeposition.InSituImmuneComplexDepositGranularpatternImmunofluorescence(IF)

GranularpatternImmunofluorescLinearpatternImmunofluorescenceLinearpatternImmunofluorescen9泌尿系統(tǒng)病理學(xué)課件1MechanismofglomerularinjuryCirculatingimmunecomplexnephritisimmunecomplexnephritisinsituCell-mediatedimmunity(sensitizedTcells)OthermechanismsMechanismofglomerularinjuryCell-MediatedImmunityinGNSensitizednephritogenicTcells,asareflectionofcell-mediatedimmunereaction,causesomeformsofglomerularinjuryandareinvolvedintheprogressionofmanyglomerulonephrities.Cell-MediatedImmunityinGNSeSummaryofpathogenesisAntibody-mediatedimmuneinjuryisanimportantmechanismofglomerulardamage,mainlyviacomplement-andleukocyte-mediatedpathways.Antibodiesmayalsobedirectlycytotoxictocellsintheglomerulus.Themostcommonformsofantibody-mediatedGNarecausedbythedepositionofcirculatingimmunecomplexesSummaryofpathogenesisAntibodStepsindiagnosesofglomerularlesionsClinicalpresentationRenalbiopsyLightmicroscopicexamination(HE，PAS，MASSON，PASMstain)ImmunofluorescenceexaminationElectronmicroscopicexamination

StepsindiagnosesofglomerulClinicalmanifestationsHematuria(redbloodcellsinurine)Proteinuria(proteinlostinurine,>3.5g/d)Oliguria(urineflow<400ml/24hours)Anuria(urineflow<100ml/24hours)EdemaHypertensionUrinarycasts(cellcasts,granularcasts,hyalinecasts)AzotemiaUremiaClinicalmanifestationsHematurAzotemiaAbiochemicalabnormalitythatreferstoanelevationofbloodureanitrogenandcreatininelevelsandlargelyrelatedtoadecreasedglomerularfiltrationrate.Prerenal;renal;postrenalAzotemiaAbiochemicalabnormalUremiaFailureofrenalexcretoryfunctionThemetabolicandendocrinealterationswithclinicalsignsandsymptomsUremicgastroenteritis,neuromusculardisorders,cardiovascularinvolvementUremiaFailureofrenalexcretoClinicalsyndromesAcutenephriticsyndrome:acuteonset,bloodpressure

，hematuria,proteinuria,edema,azotemiaRapidlyprogressivenephriticsyndrome:abruptorinsidiousonsetofhematuria,proteinuria,anemiaandrapidlyprogressingrenalfailureClinicalsyndromesAcutenephriClinicalsyndromesNephroticsyndrome:heavyproteinuria（>3.5g/d),hypoalbuminemia,severeedema,hyperlipidemiaandlipiduriaChronicnephriticsyndrome:slowlydevelopingrenalfailureaccompaniedbyproteinuria,hematuria,hypertensionanduremiaClinicalsyndromesNephroticsyRenalfailureTwotypes(acuteandchronicrenalfailure)Twomainsyndromesofpartialrenalfailure(nephriticsyndromeandnephroticsyndrome)Chronicrenalfailureisirreversible,asitiscausedbypermanentdestructionofnephronsAcuterenalfailuresometimesrecoverswhenthedamagingstimulusresolvesRenalfailureTwotypes(acutefocal<50%diffuse≥50%segmentalGlobalDistributionofbasiclesionsfocal<50%diffuse≥50%segmeBasicpathologicalchangeHypercellularityBasementmembranethickeningNecrosisHyalinizationandsclerosisBasicpathologicalchangeHyperHypercellularityHypercellularityBasementmembranethickening

Basementmembranethickening

NecrosisNecrosisHypercellularityandNecrosisHypercellularityandNecrosisHyalinizationandsclerosisHyalinizationandsclerosisPrimaryglomerulonephritisAcutediffuseproliferativeglomerulonephritisCrescenticglomerulonephritisMembranousglomerulonephritisMinimalchangeglomerulopathyFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeglomerulonephritisIgAnephropathyChronicglomerulonephritisPrimaryglomerulonephritisAcutDiffuseproliferativeglomerulonephritisDiffuse,global,acuteinflammationofglomeruliiscausedbythedepositionofimmunecomplexesinglomeruli,stimulatedbyaprecedinginfectionChildrenaremorecommonlyaffectedDiffuseproliferativeglomerulEtiologyPoststreptococcal(mostcommon):onsetis1-2weeksafteraprimaryinfectionwith-hemolyticstreptococciofgroupANon-streptococcal(lesscommon):arangeofbacterial,viralandprotozoalinfectionsEtiologyPoststreptococcal(mosMorphologyGrossexaminationSwollenwithscatteredpetechiaMorphologyGrossexaminationSwoHistologicalfeaturesEndothelialcellsproliferationMesangialcellsproliferationNeutrophilsinfiltrationHistologicalfeaturesEndotheliNormalglomerulusNormalglomerulusPost-streptococcalglomerulonephritis(HE)

Post-streptococcalglomerulonePost-streptococcalglomerulonephritis(PAS)

Post-streptococcalglomerulonePost-streptococcalglomerulonephritis(PASM)

Post-streptococcalglomeruloneImmunofluorescenceGranulardepositsC3ImmunofluorescenceGranulardepSubepithelial“humps”immunecomplexesdepositionElectronmicroscopySubepithelial“humps”immunecSubepithelial“humps”immunecomplexesdepositionSubepithelial“humps”immunecClinicalfeaturesSystemicsymptomsAcutenephriticsyndromeAcuteonset

OliguriaEdemaHypertension

Hematuria

Azotemia

InjuresofthecapillarywallGFRdecreaseFluidretentionFluidretention,reninincreasewasteproductsincreaseClinicalfeaturesSystemicsympDiffuseproliferativeglomerulonephritisCausedbyimmunecomplexesinglomerulus,oftenafterstreptococcalinfectionCausesnephriticsyndrome,withproliferationofendothelium,mesangiumandinfiltrationofneutrophilisMostcasesrecover,butaminoritymayrapidlyprogresstorenalfailureorslowlydevelopchronicrenalfailureDiffuseproliferativeglomerulPrimaryglomerulonephritisAcutediffuseproliferativeglomerulonephritisCrescenticglomerulonephritisMembranousglomerulonephritisMinimalchangeglomerulopathyFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeglomerulonephritisIgAnephropathyChronicglomerulonephritisPrimaryglomerulonephritisAcutRapidlyprogressiveglomerulonephrits(RPGN;crescenticglomerulonephritis)

RPGNisamanifestationofsevereglomerularinjurycharacterizedbytheformationofcrescent-shapedmasseswithintheBowman’sspaceRPGNoccursinasmallpercentageofpatientswithpoststreptococcalglomerulonephritis,butcanalsobeassociatedwithmanyotherformsofglomerulardamageRapidlyprogressiveglomerulonPathogenesisTypeIRPGN(12%):anti-GBMantibodies(specialtype:Goodpasturesyndrome)TypeIIRPGN(44%):immunecomplex-mediateddisorderTypeIIIRPGN(44%):pauci-immunecomplexesPathogenesisTypeIRPGN(12%):CrescenticglomerulonephritisCrescenticglomerulonephritisHistologicalfeaturesThecharacteristicisthepresenseofcrescentsinmostoftheglomeruli(>50%)ThecrescentsliningBowman’scapsulearecomposedofamixtureofepithelialcellsandmacrophagesproliferatingHistologicalfeaturesThecharaCresenticglomerulonephritisCresenticglomerulonephritisCresenticglomerulonephritisCresenticglomerulonephritis9泌尿系統(tǒng)病理學(xué)課件1CrescenticglomerulonephritisCrescent

CrescenticglomerulonephritisCBasementmembranedestruction

CresenticglomerulonephritisBasementmembranedestructionAnti-GBMdiseaseDamagetothepulmonaryalveolarcapillarybasementmembrane,producingtheclinicalfeaturesofpulmonaryhemorrhagesassociatedwithrenalfailureAnti-GBMantibodiesintheserum(plasmapheresisisuseful)GoodpasturesyndromeAnti-GBMdiseaseGoodpasturesyGoodpasturesyndromeGoodpasturesyndromeClinicalfeaturesRPGNischaracterizedbyrapidandprogressivelossofrenalfunctionassociatedwithsevereoliguriaevenanuriaPrognosisispoorClinicalfeaturesRPGNischaraPrimaryglomerulonephritisAcutediffuseproliferativeglomerulonephritisCrescenticglomerulonephritisMembranousglomerulonephritisMinimalchangeglomerulopathyFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeglomerulonephritisIgAnephropathyChronicglomerulonephritisPrimaryglomerulonephritisAcutMembranousglomerulopathyMajorcauseofnephroticsyndromeinadultsCharacterizedbyelectron-dense,immunoglobulin-containingdepositsalongtheepithelialsideoftheBM.DiffusethickeningofthecapillarywallMembranousglomerulopathyMajorMembranousglomerulopathyMembranousglomerulopathyMembranousglomerulopathyMembranousglomerulopathyMembranousglomerulopathyMembranousglomerulopathyIgGImmunofluorescence

IgGImmunofluor9泌尿系統(tǒng)病理學(xué)課件19泌尿系統(tǒng)病理學(xué)課件1ClinicalManifestationsTheconditionusuallystartsasinsidiousonsetofnephroticsyndromeorsub-nephrotic-rangeproteinuria.Upto40%ofcasesprogresstorenalinsufficiencyoveranunpredictabletimespanof2to20years.ClinicalManifestationsTheconPrimaryglomerulonephritisAcutediffuseproliferativeglomerulonephritisCrescenticglomerulonephritisMembranousglomerulonephritisMinimalchangeglomerulopathyFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeglomerulonephritisIgAnephropathyChronicglomerulonephritisPrimaryglomerulonephritisAcutMajorcauseofnephroticsyndromeinchildrenCharacterizedbynormalglomerulionlightmicroscopybutuniformanddiffuseeffacementofthefootprocessesofvisceralepithelialcellsonEMImmunofluorescenceshowsnoimmunedepositsMinimalchangedisease

MajorcauseofnephroticsyndrMinimalchangediseaseMinimalchangedisease9泌尿系統(tǒng)病理學(xué)課件19泌尿系統(tǒng)病理學(xué)課件1ClinicalmanifestationsProteinuriaisusuallyselectiveThemostcharacteristicfeatureofthisconditionisthedramaticresponsetocorticosteroidtherapyThelong-termprognosisisexcellentforchildrenandadultsClinicalmanifestationsProteinPrimaryglomerulonephritisAcutediffuseproliferativeglomerulonephritisCrescenticglomerulonephritisMembranousglomerulonephritisMinimalchangeglomerulopathyFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeglomerulonephritisIgAnephropathyChronicglomerulonephritisPrimaryglomerulonephritisAcutFocalsegmentalglomerulosclerosis

(FSGS)Characterizedbysclerosisofsegmentoftheglomeruli,andonlyaffectedfocalglomeruli(<50%)Accountsfor10%and15%ofcasesofnephroticsyndromeinchildrenandadults,respectivelyFocalsegmentalglomerulosclerFSGSFSGSFSGSFSGSFSGSFSGSIgMIFIgMIFClinicalmanifestationsAhigherincidenceofhematuria,reducedGFR,andhypertensionProteinuriaismoreoftennonselectiveRespondpoorlytocorticosteroidtherapyManyprogresstochronicglomerulonephritisClinicalmanifestationsAhighePrimaryglomerulonephritisAcutediffuseproliferativeglomerulonephritisCrescenticglomerulonephritisMembranousglomerulonephritisMinimalchangeglomerulopathyFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeglomerulonephritisIgAnephropathyChronicglomerulonephritisPrimaryglomerulonephritisAcutMembranoproliferativeglomerulonephritisLobularGN，hypocomplementGNProliferationofmesangialcellsandmatrix，basementmembraneshowsadoublecontouror“tramtrack”appearancehypocomplementemiaiscommonMembranoproliferativeglomerulMembranoproliferativeglomerulonephritisMembranoproliferativeglomerul9泌尿系統(tǒng)病理學(xué)課件19泌尿系統(tǒng)病理學(xué)課件1IgG

IFIgGIF9泌尿系統(tǒng)病理學(xué)課件19泌尿系統(tǒng)病理學(xué)課件1MembranoproliferativeglomerulonephritisChildrenandadultsadoublecontouror“tramtrack”appearanceNephroticsyndrome(~50%)，acutenephriticsyndrome,chronicnephriticsyndrome，hematuria，hypocomplementemiaiscommonPrognosisispoorMembranoproliferativeglomerulNephroticsyndromeThemostcommontypeofrenalsyndromesHeavyproteinuriainjurytoGBMandincreasedpermeabilitytotheplasmaproteinHypoalbuminemialargeexcretionoftheproteinandserumalbumindepletedEdemadropinosmoticpressureandretentionofwaterandsaltHyperlipidemiaandlipiduriaobscure,increasedsynthesisoflipoproteinbyliverNephroticsyndromeThemostcomPrimaryglomerulonephritisAcutediffuseproliferativeglomerulonephritisCrescenticglomerulonephritisMembranousglomerulonephritisMinimalchangeglomerulopathyFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeglomerulonephritisIgAnephropathyChronicglomerulonephritisPrimaryglomerulonephritisAcutIgAnephropathy

ThemostcommonGNworldwideCharacterizedbymesangialproliferationandIgAdepositionDefectsinregulationofIgAsynthesis,secretion,orclearancehavebeenpostulatedinthepathogenesisIgAnephropathy

ThemostcommoIgAnephropathy

(PAS)IgAnephropathy(PAS)IgAnephropathy(PASM)IgAnephropathy(PASM)

IgAImmunofluorescenceIgAImmunofluorescence

IgAImmunofluorescence

IgAImmunofluorescence9泌尿系統(tǒng)病理學(xué)課件19泌尿系統(tǒng)病理學(xué)課件1ClinicalmanifestationsAmajorcauseofrecurrentglomerularhematuriaAlthoughmostpatientshaveaninitialbenigncourse,chronicrenalfailuredevelopsinupto50%overaperiodof20yearsClinicalmanifestationsAmajorPrimaryglomerulonephritisAcutediffuseproliferativeglomerulonephritisCrescenticglomerulonephritisMembranousglomerulonephritisMinimalchangeglomerulopathyFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeglomerulonephritisIgAnephropathyChronicglomerulonephritisPrimaryglomerulonephritisAcutChronicglomerulonephritisEndstagekidneyItmaybecausedbymanydiseases

ChronicglomerulonephritisEndMorphologyMacroscopically,affectedkidneysaresmallandthereisgranularityofexternalsurface(symmetricallycontracted)“granularnephrosclerosis”Microscopically,thereisfibrosisandhyalinizationofglomeruli,tubularatrophyandinterstitialfibrosisMorphologyMacroscopically,affChronicglomerulonephritisChronicglomerulonephritisChronicrenalfailureChronicrenalfailureEndstagekidneyEndstagekidney9泌尿系統(tǒng)病理學(xué)課件1ClinicalfeaturesChronicglomerulonephritisdevelopsinsidiouslyChronicglomerulonephritisischaracterizedbychronicnephriticsyndromeHypertensionProteinuriaAnemiaAzotemiaUremia

EdemaClinicalfeaturesChronicglomeUremicpericarditis

“Corvillosum”Uremicpericarditis“CorviSummaryAcutediffuseproliferativeGN

acutenephriticsyndromeRapidlyprogressiveGN

rapidlyprogressivenephriticsyndromeMembranousGNMinimalchangediseaseFocalsegmentalglomerulosclerosis(FSGS)MembranoproliferativeGN

nephroticsyndromeIgAnephropathyasymptomatichematuriawithorwithoutproteinuriaChronicGN

chronicnephriticsyndromeSummaryAcutediffuseprolifer9泌尿系統(tǒng)病理學(xué)課件1CasestudyA13-year-oldgirlwhoisbroughtbyherparentsbecauseshehadbecomelethargicandherfaceappearedswollen,particularlyaroundhereyes.Onenquiry,shehadrecentlyrecoveredfromaflu-likeillness.AspartofroutineexaminationherurineistestedandisfoundthatcontainbothproteinandRBCCasestudyA13-year-oldgirlwCasestudySheisalsonotedtohaveamildlyraisedbloodpressure.Thepatientisreferredtohospitalwheresheisfoundtohaveelevatedureaandcreatininetogetherwithareducedurineoutput.Renalbiopsyisperformed.CasestudySheisalsonotedtoHistologyThehistologyreportrevealshypercellularityofglomeruliwithneutrophilsincapillarylumen.GranulardepositionofIgGandC3areseenintheGBM.EMconfirmsthepresenceofelectrondensedepositsalongthebasementmembrane,predominantlyinasubepitheliallocation.HistologyThehistologyreport9泌尿系統(tǒng)病理學(xué)課件1Questions

Whatisyourdiagnosis?Whatistheconcomitantclinicalsyndrome?AcutediffuseproliferativeGNacutenephriticsyndromeQuestionsAcutediffuseprolifOutlineGlomerulonephritis(GN)TubulointerstitialnephritisUrinaryoutflowobstructionTumorsofurinarysystemProstateDisease,TestisandPenisTumorOutlineGlomerulonephritis(GN)TubulointerstitialnephritisTubulointerstitialnephritisreferstoagroupofinflammatorydiseasesofthekidneysthatprimarilyinvolvetheinterstitumandtubulesTubulointerstitialnephritisTuTubulointerstitialnephritisPyelonephritisAcutetubularnecrosisInterstitialnephritisTubulointerstitialnephritisPyPyelonephritisAffectingtubulesAffectinginterstitumAffectingrenalpelvisOneofthemostcommondiseasesofthekidneyPyelonephritisAffectingtubuleRiskfactorsInjurytomucosaofurinarytractOutflowobstructionVesicoureteralrefluxandintrarenalrefluxImmunosuppressionandimmunodeficiencyRiskfactorsInjurytomucosaoPyelonephritis

AcutepyelonephritisChronicpyelonephritisPyelonephritisAcutepyelonephAcutepyelonephritisIncidenceparallelsthatofobstructivediseaseCausedbybacterialinfectionCommonsuppurativeinflammationofthekidneyandtherenalpelvisAcutepyelonephritisIncidenceAcutepyelonephritis

ChildhoodPregnancyElderlyInfancy:males>femalesPubertytomiddleage:females>malesPost-40years:males>femalesThreeagepeaks

GenderdifferencesAcutepyelonephritis

ChildhooRoutesofbacterialinfectionAscendinginfectionfromthelowerurinarytract(mostcommon):entericgram-negativerods(Escherichiacoli)Bloodstreamspreadinbacteremicorsepticemicstates:staphylococciRoutesofbacterialinfectionARouteofinfectionHematogenousinfection(descendinginfection)AscendinginfectionRouteofinfectionGrossfeatureSuppurativeinflammationCorticalabscessesMedullaryabscessesGrossfeatureSuppurativeinflaAcutepyelonephritisAcutepyelonephritisAcutepyelonephritisAcutepyelonephritisHistologicalfeature

InfiltrationoftubulesbyneutrophilsAbscessformationInterstitialedemaHistologicalfeatureInfiltratAcutepyelonephritisAcutepyelonephritis9泌尿系統(tǒng)病理學(xué)課件1Clinicalfeature

SuddenonsetPaininthebackEvidenceofsystemicinfection(chills,fever,malaise)Indicationsofbladderandurethralirritation(dysuria,urgency,frequencyofmicturition)ClinicalfeatureSuddenonsetUrinaryfindingsPyuria(whitebloodcellsandpuscellsinurine)Bacteriuria(bacteriainurine)UrinaryfindingsPyuria(whiteComplicationsandsequelaeResolutionHealingwithscarringChronicityPyonephrosisRenalpapillarynecrosisPerinephricabscessDeathinuremiaComplicationsandsequelaeResoPapillarynecrosisPapillarynecrosisPyelonephritis

AcutepyelonephritisChronicpyelonephritisPyelonephritisAcutepyelonephChronicpyelonephritisChronicpyelonephritisisdefinedasamorphologicentityinwhichpredominantlyinterstitialinflammationandscarring

oftherenalparenchymaisassociatedwithgrosslyvisiblescarringanddeformity

ofthepelvicalycealsystemAncauseofchronicrenalfailureChronicpyelonephritisChronicChronicpyelonephritisChronicobstructivepyelonephritisChronicreflux-associatedpyelonephritis(vesicoureteralreflux)ChronicpyelonephritisChronicGrossfeatureKidneysarenotequallydamagedIrregularareasofscarringMarkedcalycealdeformitiesGrossfeatureGrossfeaturenotequallydamagedIrregularareasofscarringMarkedcalycealdeformitiesChronicpyelonephritisGrossfeatureChronicpyelonephChronicpyelonephritisnotequallydamagedIrregularareasofscarringMarkedcalycealdeformitiesChronicpyelonephritisHistologicalfeatureChronicinflammatorycellsinfiltration,occasionallyneutrophilsUneveninterstitialfibrosisDilationorcontractionoftubulesGlomerulishowperiglomerularfibrosisHistologicalfeatureChronicinChronicpyelonephritisChronicpyelonephritis“Thyroidization”Dilationoftubules“Thyroidization”DilationoftClinicalfeaturesGradualonsetofrenalinsufficiencyTubulardysfunction(polyuria,nocturia)UrinarytractinfectionUremiaClinicalfeaturesGradualonsetDiagnosis

IntravenouspyelogramUrinecultureDiagnosisIntravenouspyelogra急性腎小管壞死(Acutetubularnecrosis)急性腎小管壞死(Acutetubularnecrosis9泌尿系統(tǒng)病理學(xué)課件1急性腎小管壞死急性腎小管壞死過敏性間質(zhì)性腎炎過敏性間質(zhì)性腎炎過敏性間質(zhì)性腎炎過敏性間質(zhì)性腎炎OutlineGlomerulonephritis(GN)TubulointerstitialnephritisUrinaryoutflowobstructionTumorsofurinarysystemProstateDisease,TestisandPenisTumorOutlineGlomerulonephritis(GN)UrinaryoutflowobstructionRenalstonesHydronephrosis

UrinaryoutflowobstructionRenRenalstonesUrolithiasisiscalculusformationatanylevelintheurinarycollectingsystemmostcommonsites:pelvicalycealsystemandbladderRenalstonesUrolithiasisiscaMainpredisposingfactorsIncreasedconcentrationofsoluteinurineReducedsolubilityofsoluteinurineMainpredisposingfactorsIncrEtiology

AcquiredInherited

EtiologyAcquiredRenalcalculusRenalcalculusRenalstaghorncalculusSRenalstaghorncalculusS9泌尿系統(tǒng)病理學(xué)課件19泌尿系統(tǒng)病理學(xué)課件1Fluoroscopy

UreteralcalculusFluoroscopyUreteralcalculusClinicalfeatureWithoutsymptomsRenalcolicwithnausea,vomitingandhematuriaDualacheintheloinsRecurrenturinarytractinfectionClinicalfeatureWithoutsymptoUrinaryoutflowobstructionRenalstonesHydronephrosisUrinaryoutflowobstructionRenHydronephrosis

Hydronephrosisreferstodilationoftherenalpelvisandcalyces,withaccompanyingatrophyoftheparenchyma,causedbyobstructiontotheoutflowofurineHydronephrosis

HydronephrosisRenalpelvisPelviuretericjunctionUreterBladderUrethraHydronephrosis

ObstructionofthelevelsRenalpelvisHydronephrosis

ObsMorphologyUnilateral:causedbyobstructionattheleveloftheureter,pelviuretericjunctionorrenalpelvisBilateral:causedbyobstructionofthelevelofthebladderorurethraMorphologyUnilateral:causedbHydronephrosis

HydronephrosisNormalurinarytractIntravenouspyelogram(IVP)NormalurinarytractIntravenouHydronephrosis

Intravenouspyelogram(IVP)HydronephrosisIntravenouspyHydronephrosis

(cutsurface)Hydronephrosis(cutsurface)9泌尿系統(tǒng)病理學(xué)課件1ClinicalfeatureClinicalfeaturesdependonthecauseandsiteofthelesionClinicalfeatureClinicalfeatuEffectsofhydronephrosisObstructionisremoved:renalfunctionreturnstonormalPersistenceofobstruction:atrophyofrenaltubuleswithglomerularhyalinizationandfibrosisEffectsofhydronephrosisObstrStaghorncalculusHydronephrosisAbscess

StaghorncalculusHydronephrosiOutlineGlomerulonephritis(GN)TubulointerstitialnephritisUrinaryoutflowobstructionTumorsofurinarysystemProstateDisease,TestisandPenisTumorOutlineGlomerulonephritis(GN)TumorsofurinarysystemTumorsofthekidneyTumorsofthebladderTumorsoftheureterTumorsoftheurethraTumorsofurinarysystemTumorsKeyfacts

renalcellcarcinoma80%-85%ofallprimaryrenalmalignanttumor,2%-3%ofalladultcancersMale:femaleincidenceis3:1Incidenceisgreatestinthoseover50years,andincreaseswithageRiskfactors:smokers,exposuretocadmium,geneticfactors(VHLgene,TFE3fusiongene)Keyfacts

renalcellcarcinomaCTRenalcellcarcinomaCTRenalcellcarcinomaRenalcellcarcinomaRenalcellcarcinomaRenalcellcarcinomainvadeintotherenalvein

RenalcellcarcinomainvadeinRenalcellcarcinoma(clearcelltype)Renalcellcarcinoma(clearceRenalcellcarcinoma(clearcelltype)Renalcellc