糖尿病腎病(英文)

DiabeticNephropathyStatisticalIncreaseinDiabetesInthepast20years,therehasbeenasteadyincreaseintheproportionofallpatientswithESRDwhohavediabetes.Accordingtothe1997reportoftheUSRDS,morethan40%ofallnewlytreatedpatientswithESRDhavediabetes.IncreasingInsulinTreatmentinNIDDMRenalFailureCumulativeIncidence.Chronicrenalfailurewasaslikelytodevelopatasuperimposablerateinbothdiabeticsubsets.Numbersinparenthesesindicatenumberofpatientsforeachline.Creatinineclearance.FurtherevidenceofthesimilarityincourseofdiabeticnephropathyintypeI(A)andtypeII(B)diabeteswaspresentedinRitzandStefansky’sstudyofequivalentdeteriorationincreatinineclearanceoverthecourseofadecade.糖尿病腎病的發(fā)病機(jī)理（1）腎內(nèi)血?jiǎng)恿W(xué)改變：腎內(nèi)血流動(dòng)力學(xué)改變是指腎小球高濾過及腎小球高壓。動(dòng)物實(shí)驗(yàn)，糖尿病模型建立后，即已存在腎小球的高濾過與腎小球肥大。糖尿病腎病的發(fā)病機(jī)理（1）高濾過是導(dǎo)致腎功能惡化的主要原因。在非糖尿病性5/6腎切除的動(dòng)物模型中可見腎小球系膜基質(zhì)增多，GBM增厚及節(jié)段性腎小球硬化。腎小球內(nèi)高壓是導(dǎo)致腎小球硬化的另一重要因素糖尿病腎病的發(fā)病機(jī)理（2）葡萄糖的毒性效應(yīng)高血糖可導(dǎo)致內(nèi)皮細(xì)胞，系膜細(xì)胞的結(jié)構(gòu)及功能的改變。高血糖促使系膜細(xì)胞合成更多的胞外基質(zhì)。持續(xù)的高血糖可使血漿蛋白及組織蛋白糖基化，導(dǎo)致晚期糖基化終末產(chǎn)物的生成。糖尿病腎病的臨床表現(xiàn)Ⅰ型及Ⅱ型糖尿病患者都有很大的可能發(fā)展為糖尿病腎病，Ⅰ型糖尿病患者其腎病更為顯著，進(jìn)展也更為迅速，當(dāng)發(fā)生了明顯糖尿病腎病后，兩型的臨床表現(xiàn)則無很大差別。臨床上按照病理生理特點(diǎn)將Ⅰ型糖尿病腎病分為Ⅰ—Ⅴ期。目前尚無Ⅱ糖尿病腎病的臨床分期，但其發(fā)生糖尿病腎病時(shí)也大體經(jīng)歷高濾過，正常白蛋白尿，微量白蛋白尿，臨床糖尿病腎病及慢性腎功能不全等幾個(gè)階段。StagesofNephropathy.Theinterrelationshipsbetweenfunctionalandmorphologicmarkersofthestagesofdiabeticnephropathyareshown.Additionalpathologicstudiesareneededtotimewithprecisionexactlywhenglomerularbasementmembrane(GBM)thickeningandglomerularmesangialexpansiontakeplace.DiabeticNephropathyinTypesI&II.WhereasmicroalbuminuriaandglomerularhyperfiltrationaresubtlepathophysiologicmanifestationsofearlyDN,transformationtoovertclinicalDNtakesplaceovermonthstomanyyears.Whilenotallmicroalbuminuricindividualsprogresstoproteinuriaandazotemia,themajorityareatriskforESRDduetoDN.糖尿病腎病及慢性腎功能不全的預(yù)防控制血糖控制血壓低蛋白飲食對(duì)AGES的治療Clinicalrecognitionofdiabeticnephropathy.Thetimingofreno-protectivetherapyindiabetesisasubjectofcurrentinquiry.Certainly,hypertension,poormetabolicregulation,andhyperlipidemiashouldbeaddressedineverydiabeticindividualatdiscovery.DiscoveryofmicroalbuminuriaisbyconsensusreasontostarttreatmentwithanACEIineithertypeofdiabetes,regardlessofBPelevation.However,nearlytheentirecourseofrenalinjuryindiabetesisclinicallysilent.Medicalinterventionduringthis“silentphase,”comprisingBPpressureregulation,metaboliccontrol,dietaryproteinrestriction,andadministrationofACEIisrenoprotective,asjudgedbyslowedlossofGFR.PROGRESSIONOFCOMORBIDITY

INTYPEIIDIABETES

COMORBIDITYINDEX

HEARTDISEASEComplicationsInitial%Subsequent%Retinopathy50100Cardiovascular4590Cerebrovascular3070Peripheralvascular1550Creatinineclearancedeclinedfrom81mL/minover74(40—119)mo.Endpoint:dialysisordeath.HEARTDISEASE

HyperlipidemiaHypertensionVolumeoverloadACEinhibitorErythropoietinHeartdiseaseis