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Article: Future directions in the treatment of IgA nephropathy

TitleFuture directions in the treatment of IgA nephropathy
Authors
Keywordsangiotensin-converting enzyme inhibitor
charge
IgA
interleukin 8
mesangium
neutrophils
platelet-derived growth factor
reactive oxygen species
sclerosis
transforming growth factor-β
Issue Date1997
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEP
Citation
Nephrology, 1997, v. 3 n. 1, p. 123-129 How to Cite?
AbstractIn IgA nephropathy (IgAN), there is a defect of clearance of immune complexes. Some of these patients ate genetically predisposed to the development of the nephritis. Poorly solubilized polymeric IgA immune complexes are then deposited in the mesangium. Recent data indirectly suggest IgA-immune complexes from patients with IgAN are different from those of healthy subjects and they can exert pathophysiologic effect on target cells. Mesangial reactivity to the immune complexes triggers off release of cytokines, with decreased prostaglandin E2 synthesis and increase in thromboxane A2 production promoting mesangial cell proliferation. Angiotensin II (ATII)-induced mesangial cell contraction with efferent arteriolar vasodilatation initiates glomerular injury and may eventually lead to glomerulosclerosis due to increased synthesis of transforming growth factor- β (TGF-β) and platelet-derived growth factor PDGF). This paper highlights the possible therapeutic strategies in the future based on the recently reported pathogenetic findings in IgAN. These strategies include: (i) decreasing the synthesis of IgA-immune complexes; (ii) limiting the mesangial uptake of IgA-immune complexes; (iii) antagonizing the effect of PDGF and TGF-β to reduce mesangial proliferation and glomerulosclerosis; and (iv) reducing the noxious glomerular injury due to infiltrating neutrophils. The effective treatment of IgAN requires a further clarification of the pathogenesis of the nephropathy. Future therapeutic attempts to slow down the rate of renal deterioration in IgAN rest on the better understanding of the mechanisms mediating inflammatory injury in the kidney.
Persistent Identifierhttp://hdl.handle.net/10722/77389
ISSN
2015 Impact Factor: 1.796
2015 SCImago Journal Rankings: 0.894
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:31:22Z-
dc.date.available2010-09-06T07:31:22Z-
dc.date.issued1997en_HK
dc.identifier.citationNephrology, 1997, v. 3 n. 1, p. 123-129en_HK
dc.identifier.issn1320-5358en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77389-
dc.description.abstractIn IgA nephropathy (IgAN), there is a defect of clearance of immune complexes. Some of these patients ate genetically predisposed to the development of the nephritis. Poorly solubilized polymeric IgA immune complexes are then deposited in the mesangium. Recent data indirectly suggest IgA-immune complexes from patients with IgAN are different from those of healthy subjects and they can exert pathophysiologic effect on target cells. Mesangial reactivity to the immune complexes triggers off release of cytokines, with decreased prostaglandin E2 synthesis and increase in thromboxane A2 production promoting mesangial cell proliferation. Angiotensin II (ATII)-induced mesangial cell contraction with efferent arteriolar vasodilatation initiates glomerular injury and may eventually lead to glomerulosclerosis due to increased synthesis of transforming growth factor- β (TGF-β) and platelet-derived growth factor PDGF). This paper highlights the possible therapeutic strategies in the future based on the recently reported pathogenetic findings in IgAN. These strategies include: (i) decreasing the synthesis of IgA-immune complexes; (ii) limiting the mesangial uptake of IgA-immune complexes; (iii) antagonizing the effect of PDGF and TGF-β to reduce mesangial proliferation and glomerulosclerosis; and (iv) reducing the noxious glomerular injury due to infiltrating neutrophils. The effective treatment of IgAN requires a further clarification of the pathogenesis of the nephropathy. Future therapeutic attempts to slow down the rate of renal deterioration in IgAN rest on the better understanding of the mechanisms mediating inflammatory injury in the kidney.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.rightsNephron. Copyright © S Karger AG.en_HK
dc.subjectangiotensin-converting enzyme inhibitoren_HK
dc.subjectchargeen_HK
dc.subjectIgAen_HK
dc.subjectinterleukin 8en_HK
dc.subjectmesangiumen_HK
dc.subjectneutrophilsen_HK
dc.subjectplatelet-derived growth factoren_HK
dc.subjectreactive oxygen speciesen_HK
dc.subjectsclerosisen_HK
dc.subjecttransforming growth factor-βen_HK
dc.titleFuture directions in the treatment of IgA nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0028-2766&volume=92&spage=263&epage=270&date=2002&atitle=Future+Directions+in+the+Treatment+of+IgA+Nephropathyen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid12218302-
dc.identifier.scopuseid_2-s2.0-8244228683en_HK
dc.identifier.hkuros81638en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-8244228683&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue1en_HK
dc.identifier.spage123en_HK
dc.identifier.epage129en_HK
dc.identifier.isiWOS:000178174500003-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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