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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(guò)敏性間質(zhì)性腎炎過(guò)敏性間質(zhì)性腎炎過(guò)敏性間質(zhì)性腎炎過(guò)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
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