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)病機理（1）腎內血動力學改變：腎內血流動力學改變是指腎小球高濾過及腎小球高壓。動物實驗，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)病機理（1）高濾過是導致腎功能惡化的主要原因。在非糖尿病性5/6腎切除的動物模型中可見腎小球系膜基質增多，GBM增厚及節(jié)段性腎小球硬化。腎小球內高壓是導致腎小球硬化的另一重要因素糖尿病腎病的發(fā)病機理（2）葡萄糖的毒性效應高血糖可導致內皮細胞，系膜細胞的結構及功能的改變。高血糖促使系膜細胞合成更多的胞外基質。持續(xù)的高血糖可使血漿蛋白及組織蛋白糖基化，導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，進展也更為迅速，當發(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防控制血糖控制血壓低蛋白飲食對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