膜性肾病伴新月体.docx
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膜性肾病伴新月体.docx
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膜性肾病伴新月体
NihonJinzoGakkaiShi.2013;55(4):
567-73.
[Acaseofcrescenticpoststreptococcalacuteglomerulonephritis(PSAGN)accompaniedbymembranousnephropathy].
[ArticleinJapanese]
MatsudaJ,NagayamaI,YamaguchiY,ItanoS,MoriD,ImakitaN,TakejiM,YamauchiA.
Source
DepartmentofGeriatricMedicineandNephrology,OsakaUniversityGraduateSchoolofMedicine,Osaka,Tokyo.
Abstract
In2010,a71-year-oldmanwasreferredtoourhospitalbecauseofmildproteinuriaandhematuria.Atthattime,hehadbeenasymptomatic.Threemonthslaterhenoticedmacroscopichematuria,followedbygeneralmalaise,andthenanorexia.Hewasadmittedforacutekidneyinjury(serumcreatinine2.7mg/dL),markedproteinuria(4.35g/gCr),andelevatedC-reactiveprotein(7.21mg/dL).Somevesicleswerenotedonthesoftpalate,andathroatcultureyieldedagrowthofgroupAbeta-hemolyticstreptococci.AntistreptolysinOandantistreptokinasetiterswereelevated,butserumcomplementlevelswerewithinnormallimits.Antineutrophilcytoplasmicantibodies(ANCA)directedagainstelastaseandbactericidalpermeabilityincreasingprotein(BPI)werepositive.Therenalfunctionandinflammationdidnotimprovedespiteoralantibiotictherapy.Pathologicalexaminationofarenalbiopsyspecimenrevealeddiffusecrescentformation,numeroussubepithelialdome-shapeddeposits(humps),andprominentendocapillaryproliferation.Furthermore,afocalandsegmentalspikeappearancewasseen,withdepositssmallerthanhumps.Therewasastrikingclinicalimprovementaftersteroidpulsetherapyfollowedbyoralprednisolone.ThefeaturesofthiscasestronglysuggestcrescenticPSAGNaccompaniedbypre-existingmembranousnephropathy.
KidneyInt.2013Aug;84
(2):
366-72.doi:
10.1038/ki.2013.55.Epub2013Feb27.
Plasmasolubleurokinasereceptorlevelsareincreasedbutdonotdistinguishprimaryfromsecondaryfocalsegmentalglomerulosclerosis.
HuangJ,LiuG,ZhangYM,CuiZ,WangF,LiuXJ,ChuR,ChenY,ZhaoMH.
Source
1]RenalDivision,PekingUniversityFirstHospital,Beijing,People'sRepublicofChina[2]InstituteofNephrology,PekingUniversity,Beijing,People'sRepublicofChina[3]KeyLaboratoryofRenalDisease,MinistryofHealthofChina,Beijing,People'sRepublicofChina[4]KeyLaboratoryofCKDPreventionandTreatment,MinistryofEducationofChina,Beijing,People'sRepublicofChina.
Abstract
Inthisstudy,wemeasuredsolubleurokinasereceptorlevels,apossiblepermeabilityfactor,intheplasmaofpatientswithprimaryfocalsegmentalglomerulosclerosis(FSGS)anddeterminedtheirassociationwithclinicalandpathologicaldatain74patientswithprimaryFSGS.Healthydonorsandpatientswithminimalchangedisease,membranousnephropathy,andsecondaryFSGSwereusedascontrols.Theplasma-solubleurokinasereceptorlevels,measuredbycommercialELISAkits,ofpatientswithprimaryFSGS(median:
2923,interquartilerange2205-4360 pg/ml)weresignificantlyhigherthanthoseofpatientswithminimalchangedisease(median2050 pg/ml),membranousnephropathy(median2029 pg/ml),andnormalindividuals(median1739 pg/ml).Therewasnosignificantdifferenceinplasma-solubleurokinasereceptorlevelsbetweenthe74patientswithprimaryand14patientswithsecondaryFSGS.Thesolubleurokinasereceptorlevelsincreasedintheorderoftipvariant,toanototherwisespecifiedvariantandacellularvariant.ThesolubleurokinasereceptorlevelsweresignificantlybutnegativelycorrelatedwithcreatinineclearanceatpresentationbutpositivelycorrelatedwithcrescentformationinpatientswithprimaryFSGS.Duringfollow-up,receptorlevelsdecreasedsignificantlyinpatientswithcompleteremission.Thus,plasma-solubleurokinasereceptorlevelsdidnotdifferentiateprimaryandsecondaryFSGS,andalthoughsignificantlyelevatedinFSGS,theyshowedconsiderableoverlapwithotherglomerulardiseases.
IndianJNephrol.2012Sep-Oct;22(5):
370–373.
doi:
10.4103/0971-4065.103924
PMCID:
PMC3544060
Transformationofmembranousintoanti-GBMnephritis
S.Imtiaz,A.Alswaida,1H.Rehman,1N.Faraz,1T.Afshan,1H.Alkafoury,1S.Qayyum,1andM.ALKhoiter1
DepartmentofMedicine,KingKhalidUniversity,HospitalRiyadh,SaudiArabia
1DepartmentofNephrology,KingKhalidUniversity,HospitalRiyadh,SaudiArabia
Addressforcorrespondence:
Dr.SalmanImtiaz,DepartmentofMedicine,KingKhalidUniversityHospital,(38),P.O.BOX2925,Postalcode11461,Riyadh,SaudiArabia.E-mail:
salman_imtiaz@
Authorinformation►CopyrightandLicenseinformation►
Copyright:
©IndianJournalofNephrology
Thisisanopen-accessarticledistributedunderthetermsoftheCreativeCommonsAttribution-Noncommercial-ShareAlike3.0Unported,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperlycited.
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Abstract
Membranousnephropathyisacommonglomerulardisease.Wereporta50-year-oldmanwithahistoryofmembranousnephropathyinremission,whopresentedwithacutekidneyinjury,proteinuria,hematuria,andhypertension.Healsohadahighanti-glomerularbasementmembrane(anti-GBM)antibodytiterandcrescenttransformationofprimarypathology.Thekidneyfunctionsdeterioratedrapidlydespiteaggressivetherapywithcyclophosphamide,methylprednisolone,andplasmapheresis.
Keywords:
Anti-glomerularbasementmembranenephritis,crescenticglomerulonephritis,membranousnephropathy,schistosomalglomerulopathy
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Introduction
Membranousnephropathyaccountsforaboutone-thirdofcasesofadultglomerulardiseases[1]andisoneoftheleadingcausesofend-stagerenaldisease(ESRD).Despiteitsfavorableprognosis,duetoitsinherenttendencyofspontaneousremissioninupto30%ofpatients,[2]thenumberofdeathsduetomembranousdiseaseishighduetoincreasingnumberofpatientswithmembranousnephropathy.[3]
Crescentictransformationofmembranousnephropathyisrare,andmaybeassociatedwithanti-glomerularbasementmembrane(anti-GBM)disease[4]ANCA-associatedcrescentictransformation,[5]ormaybewithoutanyassociation.[6]Ifnotdiagnosedearlyandtreatedaggressively,itmightresultinESRDordeath.[7]
Theetiologyandpathogenesisofthetransformationarepoorlyunderstood,andmostoftheobservationsarehypothetical.
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CaseReport
A50-year-oldmanwasreferredtoourhospital3yearsagowithahistoryofbloodydiarrheaalongwithcentralabdominalpainofcolickynature.Theclinicalexaminationwasnormalexceptforpalloranddiffusetendernessintheleftflank.Investigationsshowedahemoglobinof16.3g/dL,WBC10,700(neutrophilcount51.9%,lymphocytes22.5%,monocytes8.2%,eosinophil16.95%,basophil0.5%),platelets1,70,000/mm3,ESR101mm/h,bloodsugar90mg/dL,urea15.5mg/dL,creatinine0.70mg/dL,Na136meq/L,K4.8meql/L,andCl104meq/L.UrinalysisshowedapH5.8,protein+1,blood+3,Hb+3,RBCs30,andnoWBCs.SerologyshowedhepatitisHBsAgnegative,hepatitisCantibodynonreactive,andschistosomalantibodytiter1:
4196.
Thepatienthadundergoneacolonoscopyataprivatehospital1weekpriortovisitingus,whichreportedthepresenceofschistosomalovaalongwithmultiplepolyps.Anothercolonoscopyatourhospitalalsogavethesameresults.Twoofthepolypswereresectedandhistopathologyreportconfirmedthepresenceoftubulovillousadenomawithnoevidenceofmalignancy.Hewastreatedwithoralpraziquantel.
Amonthlaterhewasreadmittedwithpainintheleftlumberregion,whichwasdullandpersistentinnature,withnohistoryofbloodinstoolandnochangeinthecolorofurine.Anexaminationshowedapalpableleftkidneywithtendernessondeeppalpationalongwithbilateralpedaledema.Akidneyultrasoundalsoshowedenlargementofbothkidneyswithnohydronephrosis.Acomputerizedtomographic(CT)scanoftheabdomenrevealedleftrenalveinthrombosisandotherlaboratoryfindingswereessentiallyasbefore.
HisserologywasdonewhichshowedANAandAnti-dsDNAwasnegative;complementC31.6,C40.588,HepBsAg,andhepatitisCantibodywerenegative;factorVLeidenmutationnegative;prothrombinmutationnegative;proteinC75(70-140),proteinS55(65-140),anti-thrombinIII61(80-120).VDRLnegative,rheumatoidfactornegative,anti-CCPantibodynegative,Smithantibodynegative,SjögrenAnegative,andSjögrenBnegative.Twenty-fourhoursurinaryproteinwas14g.
Kidneybiopsyshowed10glomeruli,oneofwhichwascompletelysclerosed,theremainingshowedrigidityofthecapillarywall[Figure1].Therewasnocrescentformationorfibrinoidnecrosis.Tubulesandvesselsshowednosignificantpathology,whileinterstitiumshowedmildmononuclearinflammatorycellinfiltrationandtherewasnosignificantfibrosis.Immunofluorescencestudyshowedeightglomeruliwith+3granularmembranepositivitywithIgGandC3andalsotherewasfocal1+positivitywithIgM,whilefibrinogenandIgAwerenegative.Electronmicroscopyshowedsubepithelialdensedeposits[Figure2].Alltheresultsconfirmedthediagnosisofmembranousnephropathy.
Figure1
Electronphotomicrographshowingdiffusefusionofepithelialfootprocessesandwidespreadsubepithelialdensedeposit
Figure2
Sectionofaglomeruluswithaminimallythickenedbasementmembrane(PASstain,×40)
Oralanticoagulant,prednisolone30mgwithcyclosporin150mgtwiceadaywasstarted.Afollow-upcolonoscopywasperformedtwiceeach6monthsapartthatrevealedadenomatouspolypswithnoevidenceofmalignancy.Onfollow-upafter6months,hewasstablewithmildpedaledema,urea35mg/dL,creatinine0.82mg/dL,Na139meq/L,K4.9meq/L.Urinalysisshowedprotein+2,RBCnil,and24-hurinary
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