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Article: Gene polymorphism in IgA nephropathy

TitleGene polymorphism in IgA nephropathy
Authors
KeywordsGene polymorphism association
Immunoglobulin A nephropathy
Progression genes
Susceptibility genes
Issue Date2001
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEP
Citation
Nephrology, 2001, v. 6 n. 2, p. 63-70 How to Cite?
AbstractIgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. Since its original description in 1968, a large body of clinical, epidemiological and immunological studies of its pathogenesis has emerged. However, the basic molecular mechanisms of abnormal mesangial IgA deposition have remained obscure. In recent years, much clinical and experimental evidence has indicated the presence of genetic factors in the development and progression of IgAN. The search for susceptibility loci has centred on the major histocompatibility complex (MHC) using disease association in family and population studies. In addition, genes outside the realm of the MHC have been reported. The evidence for genetic factors in the onset and progression of IgAN is reviewed in this paper. The major loci influencing disease susceptibility include HLA-DR4, -DQw7 and -DQβ, C4 null and T-cell receptor Cα genes, whereas those affecting the natural course of IgAN include HLA-DQβ, angiotensin-converting enzyme D/D, T-cell receptor Cβ and endothelial cell nitric oxide synthase 4a alleles.
Persistent Identifierhttp://hdl.handle.net/10722/76641
ISSN
2015 Impact Factor: 1.796
2015 SCImago Journal Rankings: 0.894
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, Sen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:23:23Z-
dc.date.available2010-09-06T07:23:23Z-
dc.date.issued2001en_HK
dc.identifier.citationNephrology, 2001, v. 6 n. 2, p. 63-70en_HK
dc.identifier.issn1320-5358en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76641-
dc.description.abstractIgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. Since its original description in 1968, a large body of clinical, epidemiological and immunological studies of its pathogenesis has emerged. However, the basic molecular mechanisms of abnormal mesangial IgA deposition have remained obscure. In recent years, much clinical and experimental evidence has indicated the presence of genetic factors in the development and progression of IgAN. The search for susceptibility loci has centred on the major histocompatibility complex (MHC) using disease association in family and population studies. In addition, genes outside the realm of the MHC have been reported. The evidence for genetic factors in the onset and progression of IgAN is reviewed in this paper. The major loci influencing disease susceptibility include HLA-DR4, -DQw7 and -DQβ, C4 null and T-cell receptor Cα genes, whereas those affecting the natural course of IgAN include HLA-DQβ, angiotensin-converting enzyme D/D, T-cell receptor Cβ and endothelial cell nitric oxide synthase 4a alleles.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEPen_HK
dc.relation.ispartofNephrologyen_HK
dc.subjectGene polymorphism associationen_HK
dc.subjectImmunoglobulin A nephropathyen_HK
dc.subjectProgression genesen_HK
dc.subjectSusceptibility genesen_HK
dc.titleGene polymorphism in IgA nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1320-5358&volume=6&spage=63&epage=70&date=2001&atitle=Gene+polymorphism+in+IgA+nephropathyen_HK
dc.identifier.emailTang, S: scwtang@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityTang, S=rp00480en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1440-1797.2001.00033.xen_HK
dc.identifier.scopuseid_2-s2.0-0035052136en_HK
dc.identifier.hkuros63970en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035052136&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue2en_HK
dc.identifier.spage63en_HK
dc.identifier.epage70en_HK
dc.identifier.isiWOS:000169756800003-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridTang, S=7403437082en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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