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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP-
dc.contributor.authorTESTAGROSSA, Leonardo-
dc.contributor.authorAZEVEDO NETO, Raymundo-
dc.contributor.authorRESENDE, Aline-
dc.contributor.authorWORONIK, Viktoria-
dc.contributor.authorMALHEIROS, Denise-
dc.date.accessioned2013-09-23T16:44:33Z-
dc.date.available2013-09-23T16:44:33Z-
dc.date.issued2013-
dc.identifier.citationNEPHROLOGY DIALYSIS TRANSPLANTATION, v.28, n.1, p.91-98, 2013-
dc.identifier.issn0931-0509-
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/2187-
dc.description.abstractBackground. Focal segmental glomerulosclerosis (FSGS) is the most prevalent primary glomerulopathy in Brazil and its incidence is increasing worldwide. Pathogenesis is related to podocyte injury, which may be due to several factors including viruses, drugs, immunology. In 2004, the Columbia classification of FSGS identified five histologic variants of the disease: collapsing (COL), usual (not otherwise specified, NOS), tip lesion (TIP), perihilar (PHI) and cellular variant (CEL). Several studies have demonstrated molecular changes in podocytes of FSGS patients. This study sought to classify a large series of FSGS biopsies according to the Columbia classification and analyze the occurrence of immunohistochemical differences among the five variants. Methods. Approximately 131 cases of renal biopsies with a diagnosis of primary FSGS during the period from 1996-2006 were classified according to the criteria of Columbia and were then submitted to immunohistochemical staining to the following antibodies: CD10, WT-1, Vimentin, Synaptopoclin, alpha-actinin-4, GLEPP-1, cytokeratin (CK) 8-18, CK19 and Ki-67. Results. The FSGS classification resulted in 38.2% of NOS variant, in 36.6% COL, in 14.5% TIP, in 6.9% PHI and in 3.8% CEL. COL variant distinguished themselves among the others for having loss of expression of CD10, WT1 and alpha-actinin-4 (P < 0.05). Furthermore, COL gained expression of the CK8-18 and CK19 diverging from the other variants (P < 0.05). Conclusions. COL variant of FSGS presented immunohistochemical characteristics that distinguished it from others pointing to additional studies in this area. The distinct immunohistochemical properties of COL might be of help in the comprehension of this aggressive form of FSGS.-
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo-FAPESP-
dc.language.isoeng-
dc.publisherOXFORD UNIV PRESS-
dc.relation.ispartofNephrology Dialysis Transplantation-
dc.rightsrestrictedAccess-
dc.subjectfocal segmental glomerulosclerosis-
dc.subjectFSGS-
dc.subjectvariants of FSGS-
dc.subjectpodocytes-
dc.subjectimmunohistochemistry-
dc.subjectcollapsing FSGS-
dc.subject.othercollapsing glomerulopathy-
dc.subject.othernephrotic syndrome-
dc.subject.otherrenal biopsy-
dc.subject.otherdiseases-
dc.subject.otherglomerulonephritis-
dc.subject.otherpodocytopathies-
dc.subject.otheralpha-actinin-4-
dc.subject.otherfeatures-
dc.subject.othertherapy-
dc.subject.otherbiology-
dc.titleImmunohistochemical expression of podocyte markers in the variants of focal segmental glomerulosclerosis-
dc.typearticle-
dc.rights.holderCopyright OXFORD UNIV PRESS-
dc.identifier.doi10.1093/ndt/gfs325-
dc.identifier.pmid22859792-
dc.subject.wosTransplantation-
dc.subject.wosUrology & Nephrology-
dc.type.categoryoriginal article-
dc.type.versionpublishedVersion-
hcfmusp.description.beginpage91-
hcfmusp.description.endpage98-
hcfmusp.description.issue1-
hcfmusp.description.volume28-
hcfmusp.origemWOS-
hcfmusp.origem.idWOS:000315540100019-
hcfmusp.origem.id2-s2.0-84872229572-
hcfmusp.publisher.cityOXFORD-
hcfmusp.publisher.countryENGLAND-
hcfmusp.relation.referenceAlbaqumi M, 2008, J AM SOC NEPHROL, V19, P1276, DOI 10.1681/ASN.2007080926-
hcfmusp.relation.referenceBahiense-Oliveira M, 2004, CLIN NEPHROL, V61, P90-
hcfmusp.relation.referenceBariety J, 2006, J AM SOC NEPHROL, V17, P2770, DOI 10.1681/ASN.2006040325-
hcfmusp.relation.referenceBariety J, 2005, KIDNEY INT, V68, P1109, DOI 10.1111/j.1523-1755.2005.00503.x-
hcfmusp.relation.referenceBarisoni L, 1999, J AM SOC NEPHROL, V10, P51-
hcfmusp.relation.referenceBarisoni L, 2007, CLIN J AM SOC NEPHRO, V2, P529, DOI 10.2215/CJN.04121206-
hcfmusp.relation.referenceBarisoni L, 2009, ARCH PATHOL LAB MED, V133, P201, DOI 10.1043/1543-2165-133.2.201-
hcfmusp.relation.referenceChun MJ, 2004, J AM SOC NEPHROL, V15, P2169, DOI 10.1097/01.ASN.0000135051.62500.97-
hcfmusp.relation.referenceDAGATI V, 1994, KIDNEY INT, V46, P1223, DOI 10.1038/ki.1994.388-
hcfmusp.relation.referenceD'Agati VD, 2004, AM J KIDNEY DIS, V43, P368, DOI 10.1053/j.ajkd.2003.10.024-
hcfmusp.relation.referenceDijkman H, 2005, KIDNEY INT, V68, P1562, DOI 10.1111/j.1523-1755.2005.00568.x-
hcfmusp.relation.referenceDijkman HBPM, 2006, KIDNEY INT, V70, P338, DOI 10.1038/sj.ki.5001574-
hcfmusp.relation.referenceEndlich N, 2001, J AM SOC NEPHROL, V12, P413-
hcfmusp.relation.referenceGoode NP, 2004, NEPHROL DIAL TRANSPL, V19, P844, DOI 10.1093/ndt/gfg620-
hcfmusp.relation.referenceHaas M, 2005, KIDNEY INT, V67, P1188, DOI 10.1111/j.1523-1755.2005.00188.x-
hcfmusp.relation.referenceHAAS M, 1995, AM J KIDNEY DIS, V26, P740, DOI 10.1016/0272-6386(95)90437-9-
hcfmusp.relation.referenceHaas M, 1997, AM J KIDNEY DIS, V30, P621, DOI 10.1016/S0272-6386(97)90485-6-
hcfmusp.relation.referenceKaplan JM, 2000, NAT GENET, V24, P251, DOI 10.1038/73456-
hcfmusp.relation.referenceKoop K, 2003, J AM SOC NEPHROL, V14, P2063, DOI 10.1097/01.ASN.0000078803.53165.C9-
hcfmusp.relation.referenceKorbet SM, 1998, J AM SOC NEPHROL, V9, P1333-
hcfmusp.relation.referenceMalafronte P, 2006, NEPHROL DIAL TRANSPL, V21, P3098, DOI 10.1093/ndt/gfl237-
hcfmusp.relation.referenceMeyrier AY, 1999, AM J KIDNEY DIS, V33, P801, DOI 10.1016/S0272-6386(99)70239-8-
hcfmusp.relation.referenceMiao J, 2009, NEPHROL DIAL TRANSPL, V24, P3297, DOI 10.1093/ndt/gfp338-
hcfmusp.relation.referenceOhtaka A, 2002, NEPHROL DIAL TRANSPL, V17, P11, DOI 10.1093/ndt/17.suppl_9.11-
hcfmusp.relation.referencePavenstadt H, 2003, PHYSIOL REV, V83, P253, DOI 10.1152/physrev.00020.2002-
hcfmusp.relation.referenceQUINLAN RA, 1985, ANN NY ACAD SCI, V455, P282, DOI 10.1111/j.1749-6632.1985.tb50418.x-
hcfmusp.relation.referenceShankland SJ, 2000, KIDNEY INT, V58, P674, DOI 10.1046/j.1523-1755.2000.00213.x-
hcfmusp.relation.referenceSharma M, 2004, EXP BIOL MED, V229, P85-
hcfmusp.relation.referenceSilverstein DM, 2007, CLIN J AM SOC NEPHRO, V2, P700, DOI 10.2215/CJN.00230107-
hcfmusp.relation.referenceStokes MB, 2006, KIDNEY INT, V70, P1783, DOI 10.1038//sj.ki.5001903-
hcfmusp.relation.referenceThomas DB, 2006, KIDNEY INT, V69, P920, DOI 10.1038/sj.ki.5000160-
hcfmusp.relation.referenceValeri A, 1996, KIDNEY INT, V50, P1734, DOI 10.1038/ki.1996.493-
dc.description.indexMEDLINE-
hcfmusp.remissive.sponsorshipFAPESP-
hcfmusp.citation.scopus14-
hcfmusp.scopus.lastupdate2024-04-12-
Appears in Collections:

Artigos e Materiais de Revistas Científicas - FM/MCM
Departamento de Clínica Médica - FM/MCM

Artigos e Materiais de Revistas Científicas - FM/MPT
Departamento de Patologia - FM/MPT

Artigos e Materiais de Revistas Científicas - HC/ICHC
Instituto Central - HC/ICHC

Artigos e Materiais de Revistas Científicas - LIM/01
LIM/01 - Laboratório de Informática Médica

Artigos e Materiais de Revistas Científicas - LIM/16
LIM/16 - Laboratório de Fisiopatologia Renal


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