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超顺磁氧化铁增强造影剂通过巨噬细胞进入正常及移植肾脏VIP专享VIP免费

超顺磁氧化铁增强造影剂通过巨噬细胞进入正常及移植肾脏_第1页
超顺磁氧化铁增强造影剂通过巨噬细胞进入正常及移植肾脏_第2页
超顺磁氧化铁增强造影剂通过巨噬细胞进入正常及移植肾脏_第3页
EurRadiol(2007)17:2898–2907DOI10.1007/s00330-007-0660-8MOLECULARIMAGINGOlivierHaugerNicolasGrenierColetteDeminèreCatherineLasseurYahsouDelmasPierreMervilleChristianCombeReceived:16August2006Revised:22March2007Accepted:3April2007Publishedonline:22May2007#Springer-Verlag2007USPIO-enhancedMRimagingofmacrophageinfiltrationinnativeandtransplantedkidneys:initialresultsinhumansAbstractThepurposeofthisstudywastoevaluatethedetectionandcharacterizationofmacrophageinfil-trationinnativeandtransplantedkidneysusingultrasmallsuperpara-magneticironoxideparticles(USPIO).Among21patientsinitiallyenrolled,12scheduledforrenalbiop-syforacuteorrapidlyprogressiverenalfailure(n=7)orrenalgraftrejection(n=5)completedthestudy.Threemagneticresonance(MR)ses-sionswereperformedwitha1.5-Tsystem,before,immediatelyafterand72hafteri.v.injectionofUSPIOatdosesof1.7–2.6mgofiron/kg.Signalintensitychangewasevaluatedvi-suallyandcalculatedbasedonaregionofinterest(ROI)positionedonthekidneycompartments.Histologi-calexaminationshowedcorticalmac-rophageinfiltrationinfourpatients(>5macrophages/mm2),twoinnativekidneys(proliferativeextracapillaryglomerulonephritis)andtwointrans-plants(acuterejection).Thesepatientsshoweda33±18%meancorticalsignallossonT2*-weightedimages.Intheremainingeightpatients,with<5macrophages/mm2,therewasnocorticalsignalloss.However,inthreeofthese,presentingwithischemicacutetubularnecrosis,astrong(42±18%)signaldropwasfoundinthemedullaexclusively.USPIO-en-hancedMRimagingcandemonstrateinfiltrationofthekidneysbymacro-phagesbothinnativeandtransplantedkidneysandmayhelptodifferentiatebetweenkidneydiseases.KeywordsUSPIO.Nativekidney.TransplantedkidneyIntroductionSpecificdiagnosisofmostrenaldiseases,particularlyglomerulardiseases,requirespathologicalexaminationafterpercutaneousbiopsy.Currentrenalimaging,includ-ingultrasound,computedtomography(CT)andmagneticresonance(MR)imagingdidnotprovidespecificchangesallowingeithertoclassifyaccuratelykidneydiseasesortoassesstheiracuteorchroniccharacter,whichhasatremendousimpactonmanagement.Glomerularorinterstitialinfiltrationbyinflammatorycellsisaverycommonreactiveprocessineithernativeortransplantedkidneys,andmacrophagesplayamajorrole.Macrophagesareusuallyabsentinnormalkidneys.However,migrationofbloodmonocytesintorenaltissuesoccurfrequentlyinspecificnephropathies,suchasacuteO.Hauger(*).N.GrenierServiced’ImagerieDiagnostiqueetThérapeutiquedel’Adulte,GroupeHospitalierPellegrin,PlaceAmélieRaba-Léon,33076BordeauxCedex,Francee-mail:olivier.hauger@chu-bordeaux.frTel.:+33-5-56795605Fax:+33-5-56796014O.Hauger.N.GrenierLaboratoired’ImagerieMoléculaireetFonctionnelle,ERTCNRS/UniversitéVictorSegalenBordeaux2,Bordeaux,FranceC.DeminèreServiced’Anatomo-pathologie,GroupeHospitalierPellegrin,Bordeaux,FranceC.Lasseur.Y.Delmas.P.Merville.C.CombeDépartementdeNéphrologie,GroupeHospitalierPellegrin,Bordeaux,Franceproliferativetypesofexperimentalandhumanglomerulo-nephritides,renalgraftrejection,andnon-specifickidneydiseases,suchashydronephrosis.Theirroleiscomplex,contributingtoglomerularandtubulo-interstitialinjurythroughthesecretionofvariouscytokinesandproteaseswhichinducechangesinextra-cellularmatrixandpro-gressivefibroticchanges,and,conversely,allowingtocontroltheresolutionofinflammation[1].Today,inclinicalpractice,thedegreeofmacrophageinfiltrationinthekidneycanonlybeappr...

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