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Article: Macromolecular IgA1 taken from patients with familial IgA Nephropathy or their asymptomatic relatives have higher reactivity to mesangial cells in vitro

TitleMacromolecular IgA1 taken from patients with familial IgA Nephropathy or their asymptomatic relatives have higher reactivity to mesangial cells in vitro
Authors
KeywordsCytokines
Galactose deficiency
Human mesangial cells
IgA nephropathy
Macromolecular IgA1
Multiplex IgAN family
Issue Date2009
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2009, v. 75 n. 12, p. 1330-1339 How to Cite?
AbstractMultiple cases of IgA nephropathy (IgAN) may occur in families; we compared their prognosis to sporadic cases of this disease. We isolated macromolecular IgA1 from 60 patients with familial IgAN, 91 of their asymptomatic relatives, 43 patients with sporadic IgAN (SpIgAN), 90 of their asymptomatic relatives, and 43 healthy subjects. Compared with SpIgAN patients, those with multiplex familial IgAN (MpIgAN) had more advanced renal histopathology and more galactose-deficient macromolecular IgA1 in their serum. Further, when we tested the effects of the macromolecular IgA1 on human mesangial cells in culture, we found that the macromolecular IgA1 taken from familial clusters had enhanced binding to mesangial cells and caused increased expression of interleukin-6, tumor necrosis factor-α, and monocyte chemotactic peptide-1. The macromolecular IgA1 isolated from asymptomatic relatives caused increased cytokine expression in the mesangial cells when derived from MpIgAN compared with SpIgAN or healthy controls. While these studies suggest that macromolecular IgA1 isolated from patients with MpIgAN is more pathogenic than that from patients with SpIgAN, long term follow-up will be needed to clarify the risk in asymptomatic relatives of the patients with multiplex familial disease. © 2009 International Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/59212
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Committee (Hong Kong)HKU 7697/07M
L & T Charitable Foundation
House of INDOCAFE
Funding Information:

This study was supported by the Research Grant Committee (Hong Kong) (HKU 7697/07M), and Dr Chan was partly supported by L & T Charitable Foundation and the House of INDOCAFE.

References

 

DC FieldValueLanguage
dc.contributor.authorTam, KYen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorLam, MFen_HK
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-05-31T03:45:14Z-
dc.date.available2010-05-31T03:45:14Z-
dc.date.issued2009en_HK
dc.identifier.citationKidney International, 2009, v. 75 n. 12, p. 1330-1339en_HK
dc.identifier.issn0085-2538en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59212-
dc.description.abstractMultiple cases of IgA nephropathy (IgAN) may occur in families; we compared their prognosis to sporadic cases of this disease. We isolated macromolecular IgA1 from 60 patients with familial IgAN, 91 of their asymptomatic relatives, 43 patients with sporadic IgAN (SpIgAN), 90 of their asymptomatic relatives, and 43 healthy subjects. Compared with SpIgAN patients, those with multiplex familial IgAN (MpIgAN) had more advanced renal histopathology and more galactose-deficient macromolecular IgA1 in their serum. Further, when we tested the effects of the macromolecular IgA1 on human mesangial cells in culture, we found that the macromolecular IgA1 taken from familial clusters had enhanced binding to mesangial cells and caused increased expression of interleukin-6, tumor necrosis factor-α, and monocyte chemotactic peptide-1. The macromolecular IgA1 isolated from asymptomatic relatives caused increased cytokine expression in the mesangial cells when derived from MpIgAN compared with SpIgAN or healthy controls. While these studies suggest that macromolecular IgA1 isolated from patients with MpIgAN is more pathogenic than that from patients with SpIgAN, long term follow-up will be needed to clarify the risk in asymptomatic relatives of the patients with multiplex familial disease. © 2009 International Society of Nephrology.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_HK
dc.relation.ispartofKidney Internationalen_HK
dc.subjectCytokinesen_HK
dc.subjectGalactose deficiencyen_HK
dc.subjectHuman mesangial cellsen_HK
dc.subjectIgA nephropathyen_HK
dc.subjectMacromolecular IgA1en_HK
dc.subjectMultiplex IgAN familyen_HK
dc.subject.meshChemokine CCL2 - biosynthesis - genetics-
dc.subject.meshGlomerulonephritis, IGA - complications - genetics - immunology-
dc.subject.meshImmunoglobulin A - blood - chemistry - immunology-
dc.subject.meshInterleukin-6 - biosynthesis - genetics-
dc.subject.meshMesangial Cells - immunology-
dc.titleMacromolecular IgA1 taken from patients with familial IgA Nephropathy or their asymptomatic relatives have higher reactivity to mesangial cells in vitroen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/ki.2009.71en_HK
dc.identifier.pmid19340088-
dc.identifier.scopuseid_2-s2.0-67349139414en_HK
dc.identifier.hkuros161036en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67349139414&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume75en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1330en_HK
dc.identifier.epage1339en_HK
dc.identifier.isiWOS:000266451400014-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTam, KY=25930206700en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=55182644100en_HK
dc.identifier.scopusauthoridLam, MF=35300050600en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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