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Article: Novel mechanisms of tubulointerstitial injury in IgA nephropathy: A new therapeutic paradigm in the prevention of progressive renal failure

TitleNovel mechanisms of tubulointerstitial injury in IgA nephropathy: A new therapeutic paradigm in the prevention of progressive renal failure
Authors
KeywordsAngiotensin II
Angiotensin II subtype-1 receptor
Angiotensin II subtype-2 receptor
Glomerulotubular crosstalk
IgA nephropathy
Mesangial cells
Polymeric IgA
Proximal tubular epithelial cells
Tubulointerstitial injury
Issue Date2004
PublisherSpringer Japan. The Journal's web site is located at http://link.springer-ny.com/link/service/journals/10157/index.htm
Citation
Clinical And Experimental Nephrology, 2004, v. 8 n. 4, p. 297-303 How to Cite?
AbstractIgA nephropathy (IgAN) runs a highly variable clinical course with frequent involvement of tubulointerstitial damage. Notably, renal progression correlates more closely with the severity of tubulointerstitial lesions than with the degree of glomerular lesions In IgAN. Mesangial IgA deposition induces local release of cytokines, complement, and angiotensin II leading to glomerular inflammation. It remains unclear how mesangial IgA deposition leads to tubulointerstitial injury in IgAN. Moreover, IgA deposits are rarely detected in renal interstitium in IgAN. We hypothesize that mediators released from mesangial cells triggered by IgA deposition leads to activation of proximal tubular epithelial cells. Our preliminary findings implicate a glomerulotubular cross talk with mediators released from the mesangium contributing to the pathogenesis of tubulointerstitial damage in IgAN. We have also found the expression of angiotensin II subtype-1 receptor or angiotensin II subtype-2 receptor in proximal tubular epithelial cells differs from that of mesangial cells. One potential therapeutic approach is to counterbalance the growth-stimulatory effects of angiotensin II through subtype-1 receptor in tubular epithelial cells by subtype-2 receptor-mediated apoptosis and growth inhibition. These novel findings may provide clinicians new therapeutic approach for selective blockade of the RAS in IgAN. © Japanese Society of Nephrology 2004.
Persistent Identifierhttp://hdl.handle.net/10722/77156
ISSN
2015 Impact Factor: 1.945
2015 SCImago Journal Rankings: 0.774
References

 

DC FieldValueLanguage
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:28:53Z-
dc.date.available2010-09-06T07:28:53Z-
dc.date.issued2004en_HK
dc.identifier.citationClinical And Experimental Nephrology, 2004, v. 8 n. 4, p. 297-303en_HK
dc.identifier.issn1342-1751en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77156-
dc.description.abstractIgA nephropathy (IgAN) runs a highly variable clinical course with frequent involvement of tubulointerstitial damage. Notably, renal progression correlates more closely with the severity of tubulointerstitial lesions than with the degree of glomerular lesions In IgAN. Mesangial IgA deposition induces local release of cytokines, complement, and angiotensin II leading to glomerular inflammation. It remains unclear how mesangial IgA deposition leads to tubulointerstitial injury in IgAN. Moreover, IgA deposits are rarely detected in renal interstitium in IgAN. We hypothesize that mediators released from mesangial cells triggered by IgA deposition leads to activation of proximal tubular epithelial cells. Our preliminary findings implicate a glomerulotubular cross talk with mediators released from the mesangium contributing to the pathogenesis of tubulointerstitial damage in IgAN. We have also found the expression of angiotensin II subtype-1 receptor or angiotensin II subtype-2 receptor in proximal tubular epithelial cells differs from that of mesangial cells. One potential therapeutic approach is to counterbalance the growth-stimulatory effects of angiotensin II through subtype-1 receptor in tubular epithelial cells by subtype-2 receptor-mediated apoptosis and growth inhibition. These novel findings may provide clinicians new therapeutic approach for selective blockade of the RAS in IgAN. © Japanese Society of Nephrology 2004.en_HK
dc.languageengen_HK
dc.publisherSpringer Japan. The Journal's web site is located at http://link.springer-ny.com/link/service/journals/10157/index.htmen_HK
dc.relation.ispartofClinical and Experimental Nephrologyen_HK
dc.subjectAngiotensin IIen_HK
dc.subjectAngiotensin II subtype-1 receptoren_HK
dc.subjectAngiotensin II subtype-2 receptoren_HK
dc.subjectGlomerulotubular crosstalken_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.meshDisease Progressionen_HK
dc.subject.meshEpithelial Cells - cytology - metabolismen_HK
dc.subject.meshGlomerulonephritis, IGA - pathology - therapyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoglobulin A - metabolismen_HK
dc.subject.meshKidney Failure, Chronic - prevention & controlen_HK
dc.subject.meshKidney Tubules - cytology - pathologyen_HK
dc.subject.meshReceptor, Angiotensin, Type 1 - metabolismen_HK
dc.subject.meshReceptor, Angiotensin, Type 2 - metabolismen_HK
dc.titleNovel mechanisms of tubulointerstitial injury in IgA nephropathy: A new therapeutic paradigm in the prevention of progressive renal failureen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1342-1751&volume=8&spage=297&epage=303&date=2004&atitle=Novel+mechanisms+of+tubulointerstitial+injury+in+IgA+nephropathy:+a+new+therapeutic+paradigm+in+the+prevention+of+progressive+renal+failureen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10157-004-0324-9en_HK
dc.identifier.pmid15619027-
dc.identifier.scopuseid_2-s2.0-21744462285en_HK
dc.identifier.hkuros99278en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-21744462285&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.issue4en_HK
dc.identifier.spage297en_HK
dc.identifier.epage303en_HK
dc.publisher.placeJapanen_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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