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Conference Paper: Glomerular pathology of allograft kidneys in Hong Kong

TitleGlomerular pathology of allograft kidneys in Hong Kong
Authors
Issue Date2005
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/transproceed
Citation
Transplantation Proceedings, 2005, v. 37 n. 10, p. 4293-4296 How to Cite?
AbstractAims. Our goal was to define the spectrum of glomerular diseases in allograft kidneys and to correlate them with clinical parameters. Methods. Eight hundred ninety-one renal graft biopsies and 43 graft nephrectomies from 1980 to 2004 were obtained from 442 allografts transplanted to 425 patients. Results. Glomerular diseases were diagnosed in 33% of kidney grafts. Indications for biopsy were baseline assessment (23 biopsies, 2.5%); renal dysfunction (790 biopsies, 88.7%); proteinuria (154 biopsies, 17.3%); hematuria (11 biopsies, 1.2%); and study protocol (four biopsies, 0.4%). The median time to take a biopsy was less than 8 months posttransplant. The mean time posttransplant when the biopsy diagnosis was made was 70 months for IgA nephropathy (IgAN); 66 months for transplant glomerulopathy (TG); 65 months for focal segmental glomerulosclerosis (FSG); 55 months for mesangiocapillary glomerulonephritis (MCGN); 45 months for membranous glomerulonephritis (GN); 49 months for mesangial proliferative GN; and 101 months for diabetic nephropathy. Recurrent glomerular disease was documented in 31 (7.0%) grafts. Specific glomerular diseases were diagnosed by biopsies in 106 (89.1%) of 119 proteinuric allografts. Conclusions. Glomerulopathy was common in allografted kidneys. IgAN, TG, FSG, mesangial proliferative GN, and membranous GN were the majority. A higher proportion of grafts from donors related to the recipients than from unrelated donors showed IgAN (P < .05), suggesting that genetic factors might play a role in the pathogenesis of IgAN. Recurrence of glomerulopathy underlying ESRD was frequent for IgAN, FSG, and MCGN, but this was rarely seen in membranous GN. © 2005 by Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78337
ISSN
2023 Impact Factor: 0.8
2023 SCImago Journal Rankings: 0.318
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, KWen_HK
dc.contributor.authorChan, GSWen_HK
dc.contributor.authorTang, Sen_HK
dc.date.accessioned2010-09-06T07:41:46Z-
dc.date.available2010-09-06T07:41:46Z-
dc.date.issued2005en_HK
dc.identifier.citationTransplantation Proceedings, 2005, v. 37 n. 10, p. 4293-4296en_HK
dc.identifier.issn0041-1345en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78337-
dc.description.abstractAims. Our goal was to define the spectrum of glomerular diseases in allograft kidneys and to correlate them with clinical parameters. Methods. Eight hundred ninety-one renal graft biopsies and 43 graft nephrectomies from 1980 to 2004 were obtained from 442 allografts transplanted to 425 patients. Results. Glomerular diseases were diagnosed in 33% of kidney grafts. Indications for biopsy were baseline assessment (23 biopsies, 2.5%); renal dysfunction (790 biopsies, 88.7%); proteinuria (154 biopsies, 17.3%); hematuria (11 biopsies, 1.2%); and study protocol (four biopsies, 0.4%). The median time to take a biopsy was less than 8 months posttransplant. The mean time posttransplant when the biopsy diagnosis was made was 70 months for IgA nephropathy (IgAN); 66 months for transplant glomerulopathy (TG); 65 months for focal segmental glomerulosclerosis (FSG); 55 months for mesangiocapillary glomerulonephritis (MCGN); 45 months for membranous glomerulonephritis (GN); 49 months for mesangial proliferative GN; and 101 months for diabetic nephropathy. Recurrent glomerular disease was documented in 31 (7.0%) grafts. Specific glomerular diseases were diagnosed by biopsies in 106 (89.1%) of 119 proteinuric allografts. Conclusions. Glomerulopathy was common in allografted kidneys. IgAN, TG, FSG, mesangial proliferative GN, and membranous GN were the majority. A higher proportion of grafts from donors related to the recipients than from unrelated donors showed IgAN (P < .05), suggesting that genetic factors might play a role in the pathogenesis of IgAN. Recurrence of glomerulopathy underlying ESRD was frequent for IgAN, FSG, and MCGN, but this was rarely seen in membranous GN. © 2005 by Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/transproceeden_HK
dc.relation.ispartofTransplantation Proceedingsen_HK
dc.rightsTransplantation Proceedings. Copyright © Elsevier Inc.en_HK
dc.subject.meshBiopsyen_HK
dc.subject.meshCadaveren_HK
dc.subject.meshHong Kongen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoglobulin A - blooden_HK
dc.subject.meshKidney Diseases - classification - epidemiology - immunology - pathologyen_HK
dc.subject.meshKidney Function Testsen_HK
dc.subject.meshKidney Glomerulus - immunology - pathologyen_HK
dc.subject.meshKidney Transplantation - immunology - pathologyen_HK
dc.subject.meshLiving Donorsen_HK
dc.subject.meshNephrectomyen_HK
dc.subject.meshRetrospective Studiesen_HK
dc.subject.meshTissue Donorsen_HK
dc.subject.meshTransplantation, Homologous - pathologyen_HK
dc.titleGlomerular pathology of allograft kidneys in Hong Kongen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0041-1345&volume=37&issue=10&spage=4293&epage=6&date=2005&atitle=Glomerular+pathology+of+allograft+kidneys+in+Hong+Kongen_HK
dc.identifier.emailChan, KW:hrmtckw@hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.transproceed.2005.11.001en_HK
dc.identifier.pmid16387100-
dc.identifier.scopuseid_2-s2.0-29544442418en_HK
dc.identifier.hkuros114277en_HK
dc.identifier.hkuros124480-
dc.identifier.hkuros138350-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-29544442418&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue10en_HK
dc.identifier.spage4293en_HK
dc.identifier.epage4296en_HK
dc.identifier.isiWOS:000234412900036-
dc.publisher.placeUnited Statesen_HK
dc.identifier.issnl0041-1345-

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