急性肾小球肾炎(全英班)

AcuteGlomerulonephritisPediatricdeptofTCMhospitalofGuangdongProvinceContentFamiliarwithEpidemiologyFamiliarwithDiagnosisMasterDifferentiationofsyndromeandtreatmentDescriptionofancientdoctorofTCM《灵枢·肿胀篇》:ShuizhonginTCM(edema)startfromeyelid,mildeyelidedemaasifonejustgetup,rapidpulseinneck,intermittentcough,coldfeelingbetweenperineumandthigh,edemainanteriortibialsiteandfeet,enlargedabdomen,nopittingasifwaterinit.Descriptionofwesternmedicine

EdemaHypertensionhematuriaDefinitionofAGNAcuteonsetAdisorderofagroupofglomeruliduetodifferentcausesClinicalmanifestation:hematuria,edema,proteinuria,hypertensionEpidemiologyofAGNMorbidityishighestinrenalandurogenitaldisorderEpidemiologyofAGNAcuteonsetPrevailinchildrenin3-12,especialyinschool

agepopulation,seldomseeninchildrenbelow2.MorbidityratioofM:Fis1.5~2.5:1PathogenesisofAGNinwesternmedicineGroupAβ-hemolyticstreptococci

EtiologyAGNPathogenesisGroupAβ-hemolyticstreptococci

（Ag）circulationimmunecomplexesleukocytes(release)DamageGBM

GFR↓

RetenionofwaterandNatrium

oliguriaBloodVolumeoverload

Edema

Hypertension

hematuriaproteinuriacomplementsystem(C3)Inflammationofkidneybloodcoagulationsystem(thrombus)CellProliferationEtiologyandPathogenesisofAGNinwesternmedicine

Medicalhistory：

upperrespiratorytractinfection：1~2weeksbefore，winterandspring；

skininfection

：2~3weeksbefore,summerandautumPathogenesis

Inflammationofkidneyduetocirculationimmunecomplexes

PathologyofAGN

Pathology

AGNPATHOLOGY

PASM-HE染色

×400正常

PASM染色

×100ECPGN

EtiologyofAGNinTCMSummaryExogenous：wind/dampness/soreinfectionInternal：congenitalweakphysique/acquiredweakconstitutionPathogenicfactorQuestionsMetabolismofwaterinTCMOppinion:TreeabundunceandtwoinsufficiencyPathogenesisofAGNinTCMPathogenesisETIOGYDredgewaterpassageTransportation/distributionwaterTransformationofqiWatermetabolismWaterand

dampnessaccumulatedintheskinandmuscleGivingrisetoedemaLUNGSPLEENKIDNEYClinicalmanifestationMedicalhistoryStreptococccalinfection1-3weeksbeforeonsetClinicalmanifestationSymptomsandsignsEdemaunpittingFaceandeyelid

ClinicalmanifestationSymptomsandsignsOliguriayear

normal

oliguria

anuria<1400-500<2001-3500-600<200<30-504-6600-800<3007-14800-1400<400(ml)1～2weeksClinicalmanifestationSymptomsandsignsGrosshematuriaMicroscopichematuriaClinicalmanifestationSymptomsandsignsHypertension

bloodpressure（mmHg）preschool>120/80Earlyschool>130/90（1）30%-80%cases。（2）resolveswithin1-2weeksaccopanywithincreasingofamountofurine（3）ifveryhigh，becarefulofencephalicdiseaseClinicalmanifestation

Redbloodcell++～++++RedcastProteinuria+～+++，Routineurineexamination

LaboratoryexaminationClinicalmanifestationASO

Laboratoryexamination

Positiverate50%～80%Aferinfection,ASOtitterbegintoincreasewithin2-3weeks,thesummitiswithin3-5weeks,thendecreaseslowlyin3-6months,recoverytimein1year.AnantibodytostreptococcalantigenClinicalmanifestationC3Laboratoryexamination80～90%，SerumCзdecreasewithin2weeks.recoveryafter6-8weeksCзdeterminationisveryimportanttodifferentiatebetweenAGNandothertypes

Severecondition

acutecongestiveheartfailure

hypertensiveencephalicdisease

acutekidneyfailure

earlystag（in2weeks）

Emergency，needrescueEssentialsfordignosisMedicalhistory:streptococcalinfectionlikeURIorskininfectionwithin1-3weeksClinicalmanifestation:edema,oliguria,hematuria,hypertensionLab：C3decrease,ASOincreaseSyndromedifferentiation

andtreatmentSthenia,EliminatingfirstCommonsyndromesWindandwaterstrugglingwitheachotherInternalinvasionofdampnessQideficiencyoflungandspleensupplementaryexplanation:thefirsttwosyndromescanbeseenattheearlystageofAGN,whileqideficiencyoflungand