急性腎小球腎炎(英文版)

AcuteGlomerulonephritis

急性腎小球腎炎ManycausesCommonlyafterrecentinfectionAcuteonsetAcutenephriticsyndromeHematuriaProteinuriaEdemaHypertensionRenalinsufficiency(oliguria)DefinitionCausesNon-infectious:drugs,systemicdiseasesInfectious:bacteria,virus,fungi,rickettsia,parasitesGroupAβhemolyticstreptococcal:80%-90%

“Nephritogenic”strainsofgroupAβ-hemolyticstreptococciThroat(serotype12)Coldweather51%Skin(serotype49)Warmweather25.8%EtiologyandEpidemiologyImmunecomplexesActivationofComplements,RecruitmentofleukocytesGBMdamage,BloodingredientsleakageProliferationofMCandECBlockageofrenalcapillariesGFROliguria,sodiumandwaterretention,hypervolemiaCytokinesInflammationStreptocacciInfectionPathogenesisHematuriaProteinuriaRBCCasts

EdemaHypertentionEncephalopathyRenalfailurePathologicalChangesEnlargedAllglomeruliappearenlargedandshowdiffusemesangialcellproliferationwithanincreaseinmesangialmatrix.Polymorphonuclearleukocytesarecommoninglomeruliduringtheearlystageofthedisease.Crescentsandinterstitialinflammationmaybeseeninseverecases.7A:normalglomerularcapillaryloopB:glomerularcapillaryloopofAPSGNABPathologicalChangesIFM:lumpy-bumpydepositsofimmunoglobulinandcomplementontheGBMandinthemesangium.EM:electron-densedeposits,or“humps,”areobservedontheepithelialsideoftheGBM.IFmicrographofaglomerularsegmentfromapatientwithAPSGNshowingcoarselygranularcapillarywallstainingforIgG(left)andC3(right).IFMEMEMofaportionofaglomerularcapillaryfromapatientwithAPSGNshowingsubepithelialdensedepositsandaneutrophilmarginatedagainstthebasementmembranewithnointerveningendothelialcytoplasm.

Age:5-12yrMale:female=2:1ClinicalManifestations

ClinicalManifestations

Antecedentinfection:Pharyngitis:6~12d(average10d)Pyoderma:14~28d(average20d)TypicalManifestationsEdemaHematuriaProteinuriaHypertensionOliguriaoranuriaClinicalManifestations

ClinicalManifestations

Fromasymptomaticmicroscopichematuriatooliguricacuterenalfailure15ClinicalManifestationsSevereCasesHypertensiveencephalopathyCirculatoryhypervolemiaAcuterenalfailureAtypicalManifestationAsymptomatictype

Extrarenalmanifestationtype

NephrotictypeClinicalManifestationsLaboratoryFindings

UrinalysisGFRBloodbiochemistryESRLaboratoryFindingsEvidencesofstreptococcalinfection

BacterialcultureAntistreptolysinO(ASO)Pharyngitis(80%)Skininfections(<50%).Anti-deoxyribonuclease(DNase)BPharyngitis(98%)skininfections(80%)ADPNase,HAaseLaboratoryFindings

ActivationofcomplementsSerumC3leveldecreases:80%~90%Returnstonormalwithin8wk20DiagnosisAntecedentinfectionsuddenonsetAcutenephriticsyndromeHematuria,proteinuria,cylindruria（管型尿）EdemaHypertensionRenalinsufficiencyEvidencesofstreptococcalinfectionC3levelreducesIndicationsofRenalBiopsy

AcuterenalfailureNephroticsyndromeAbsenceofevidenceofstreptococcalinfectionNormalcomplementlevelsHematuriaandproteinuria,diminishedrenalfunction,and/oralowC3levelpersistedmorethan2monthafteronsetIgAnephropathyRapidprogressiveglomerulonephritis(RPGN),GoodpasturesyndromeNephritictypenephroticsyndromeAlportsyndromeRecurrentbenignfamilialhematuriaC3NephritisDifferentialDiagnosis

Hemolytic-UremicSyndrome(HUS)Thromboticthrombocytopenicpurpura(TTP)WilsondiseaseExacerbationofchronicglomerulonephritisSecondaryglomerulonephritisDifferentialDiagnosis

TreatmentBedrestDietAntibioticsPenicillin:10-14dTreatmentDiuresisHypertensionSaltandwaterrestrictionDiuresisCalciumchannelantagonistsACEICirculatoryhypervolemiaDiureticSodiumNitroprusside（硝普鈉）PeritonealdialysisorhemofiltrationOxygenSedation（鎮(zhèn)靜）Cardiotonic（強心劑）TreatmentHypertensiveencephalopathyManagementofconvulsionDecreaseBP:sodiumNitroprusside（硝普鈉）,calciumchannelantagonistsLightenencephaledemaDiuretic,SteroidsMannitol,dextroseoralbuminareforbiddenOxygenSedation（鎮(zhèn)靜）TreatmentAcuterenalfailureManagementofhypertension,hypervolemia,electrolytesdisorderandmetabolicacidosisDialysis（透析）TreatmentTreatmentIndicationsofdialysisVolumeoverloadPersistenthyperkalemiaSeveremetabolicacidosisunresponsivetomedicalmanagementNeurologicsymptomsBUNgreaterthan100~150mg/dLCalcium/phosphor