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Conference Paper: Mechanisms of tubulointerstitial injury in IgA nephropathy

TitleMechanisms of tubulointerstitial injury in IgA nephropathy
Authors
KeywordsAngiotensin II
Angiotensin II subtype-1 receptor
Angiotensin II subtype-2 receptor
Glomerulotubular cross-talk
IgA nephropathy
Mesangial cells
Polymeric IgA
Proximal tubular epithelial cells
Tubulointerstitial injury
Issue Date2005
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, Supplement, 2005, v. 67 n. 94, p. S-110-S-115 How to Cite?
AbstractBackground. IgA nephropathy (IgAN) runs a highly variable clinical course, with frequent involvement of tubulointerstitial damage. A subgroup of IgAN with severe tubulointerstitial damage is often associated with the most rapid progression to end-stage renal failure. In IgAN, mesangial sclerosis and tubulointerstitial damage were found to be correlated with the increase in pore size of the glomerular barrier. Methods. The direct toxicity of proximal tubular epithelial cells (PTEC) by IgA in IgAN is still unresolved. Activation of PTEC by mediators released from infiltrating cells or resident kidney cells that induce tubular inflammation is the common final pathway in most chronic renal diseases. We hypothesize that mediators released from human mesangial cells (HMC) triggered by IgA deposition may lead to PTEC activation. Results. We found that IgA binding to PTEC was less than one tenth that of HMC. The binding was nonspecific and exhibited no increased cell proliferation or enhanced synthesis of cytokines or adhesion molecules. However, when PTEC were cultured with IgA-HMC spent medium prepared from IgAN patients, there was enhanced proliferation of PTEC and increased synthesis of cytokines and adhesion molecules. Conclusion. These findings implicate a glomerulotubular cross-talk with mediators released from the mesangium, contributing to the pathogenesis of tubulointerstitial damage in IgAN. There are preliminary data to suggest that the expression of angiotensin II subtype-1 receptor and angiotensin II subtype-2 receptor in PTEC differs from that of HMC. These novel findings may provide clinicians new therapeutic approach for selective blockade of the tubulointerstitial injury in IgAN. © 2005 by the International Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/76913
ISSN
2014 SCImago Journal Rankings: 0.578
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorLeung, JCKen_HK
dc.date.accessioned2010-09-06T07:26:16Z-
dc.date.available2010-09-06T07:26:16Z-
dc.date.issued2005en_HK
dc.identifier.citationKidney International, Supplement, 2005, v. 67 n. 94, p. S-110-S-115en_HK
dc.identifier.issn0098-6577en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76913-
dc.description.abstractBackground. IgA nephropathy (IgAN) runs a highly variable clinical course, with frequent involvement of tubulointerstitial damage. A subgroup of IgAN with severe tubulointerstitial damage is often associated with the most rapid progression to end-stage renal failure. In IgAN, mesangial sclerosis and tubulointerstitial damage were found to be correlated with the increase in pore size of the glomerular barrier. Methods. The direct toxicity of proximal tubular epithelial cells (PTEC) by IgA in IgAN is still unresolved. Activation of PTEC by mediators released from infiltrating cells or resident kidney cells that induce tubular inflammation is the common final pathway in most chronic renal diseases. We hypothesize that mediators released from human mesangial cells (HMC) triggered by IgA deposition may lead to PTEC activation. Results. We found that IgA binding to PTEC was less than one tenth that of HMC. The binding was nonspecific and exhibited no increased cell proliferation or enhanced synthesis of cytokines or adhesion molecules. However, when PTEC were cultured with IgA-HMC spent medium prepared from IgAN patients, there was enhanced proliferation of PTEC and increased synthesis of cytokines and adhesion molecules. Conclusion. These findings implicate a glomerulotubular cross-talk with mediators released from the mesangium, contributing to the pathogenesis of tubulointerstitial damage in IgAN. There are preliminary data to suggest that the expression of angiotensin II subtype-1 receptor and angiotensin II subtype-2 receptor in PTEC differs from that of HMC. These novel findings may provide clinicians new therapeutic approach for selective blockade of the tubulointerstitial injury in IgAN. © 2005 by the 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 International, Supplementen_HK
dc.subjectAngiotensin IIen_HK
dc.subjectAngiotensin II subtype-1 receptoren_HK
dc.subjectAngiotensin II subtype-2 receptoren_HK
dc.subjectGlomerulotubular cross-talken_HK
dc.subjectIgA nephropathyen_HK
dc.subjectMesangial cellsen_HK
dc.subjectPolymeric IgAen_HK
dc.subjectProximal tubular epithelial cellsen_HK
dc.subjectTubulointerstitial injuryen_HK
dc.subject.meshGlomerulonephritis, IGA - pathology - physiopathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshNephritis, Interstitial - pathology - physiopathologyen_HK
dc.titleMechanisms of tubulointerstitial injury in IgA nephropathyen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0085-2538&volume=67&issue=suppl 94&spage=S110&epage=S115&date=2005&atitle=Mechanisms+of+tubulointerstitial+injury+in+IgA+nephropathyen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid15752226en_HK
dc.identifier.scopuseid_2-s2.0-15944388897en_HK
dc.identifier.hkuros99484en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-15944388897&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume67en_HK
dc.identifier.issue94en_HK
dc.identifier.spageSen_HK
dc.identifier.epage110en_HK
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK

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