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Conference Paper: Mediators of inflammation and fibrosis

TitleMediators of inflammation and fibrosis
Authors
KeywordsAdipocytes
Fibrosis
Inflammation
Mesothelium
Issue Date2007
PublisherMultimed, Inc. The Journal's web site is located at http://pdiconnect.com
Citation
Peritoneal Dialysis International, 2007, v. 27 SUPPL. 2, p. S65-S71 How to Cite?
AbstractDuring peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiologic hypertonic environment with high glucose content and low pH. Current sterile dialysis solutions cause inflammation in the submesothelial compact zone, leading to fibrosis, angiogenesis, and, eventually, ultrafiltration failure. Although the normal interstitium separates the peritoneal microvasculature from the dialysis fluid and makes transperitoneal transport less efficient, changes in the submesothelial compact zone can result in progressive increases in solute transfer and ultrafiltration diminution. This peritoneal dysfunction will further be amplified with the development of an epithelial-to-mesenchymal transition of mesothelial cells and dissipation of the osmotic driving force through the increased area and solute transport that accompany neoangiogenesis of the submesothelial microvasculature.The alteration of the peritoneal membrane can be further aggravated by peritonitis, advanced glycation end-products, and glucose degradation products. Furthermore, new data are emerging to support a proinflammatory rote for peritoneal adipocytes. Copyright © 2007 International Society for Peritoneal Dialysis. Printed in Canada. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78532
ISSN
2015 Impact Factor: 1.298
2015 SCImago Journal Rankings: 0.683
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLeung, JCKen_HK
dc.date.accessioned2010-09-06T07:43:55Z-
dc.date.available2010-09-06T07:43:55Z-
dc.date.issued2007en_HK
dc.identifier.citationPeritoneal Dialysis International, 2007, v. 27 SUPPL. 2, p. S65-S71en_HK
dc.identifier.issn0896-8608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78532-
dc.description.abstractDuring peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiologic hypertonic environment with high glucose content and low pH. Current sterile dialysis solutions cause inflammation in the submesothelial compact zone, leading to fibrosis, angiogenesis, and, eventually, ultrafiltration failure. Although the normal interstitium separates the peritoneal microvasculature from the dialysis fluid and makes transperitoneal transport less efficient, changes in the submesothelial compact zone can result in progressive increases in solute transfer and ultrafiltration diminution. This peritoneal dysfunction will further be amplified with the development of an epithelial-to-mesenchymal transition of mesothelial cells and dissipation of the osmotic driving force through the increased area and solute transport that accompany neoangiogenesis of the submesothelial microvasculature.The alteration of the peritoneal membrane can be further aggravated by peritonitis, advanced glycation end-products, and glucose degradation products. Furthermore, new data are emerging to support a proinflammatory rote for peritoneal adipocytes. Copyright © 2007 International Society for Peritoneal Dialysis. Printed in Canada. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherMultimed, Inc. The Journal's web site is located at http://pdiconnect.comen_HK
dc.relation.ispartofPeritoneal Dialysis Internationalen_HK
dc.subjectAdipocytesen_HK
dc.subjectFibrosisen_HK
dc.subjectInflammationen_HK
dc.subjectMesotheliumen_HK
dc.subject.meshDialysis Solutions - adverse effectsen_HK
dc.subject.meshEpithelium - metabolism - pathologyen_HK
dc.subject.meshFibrosisen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInflammation - pathologyen_HK
dc.subject.meshInflammation Mediators - metabolismen_HK
dc.subject.meshKidney Failure, Chronic - pathology - therapyen_HK
dc.subject.meshPeritoneal Dialysis - adverse effectsen_HK
dc.subject.meshPeritoneum - metabolism - pathologyen_HK
dc.subject.meshPeritonitis - metabolism - pathologyen_HK
dc.subject.meshUltrafiltrationen_HK
dc.titleMediators of inflammation and fibrosisen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0896-8608&volume=27&spage=S65&epage=71&date=2007&atitle=Mediators+of+inflammation+and+fibrosisen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid17556333-
dc.identifier.scopuseid_2-s2.0-35748951639en_HK
dc.identifier.hkuros136609en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35748951639&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issueSUPPL. 2en_HK
dc.identifier.spageS65en_HK
dc.identifier.epageS71en_HK
dc.identifier.isiWOS:000257889500013-
dc.publisher.placeCanadaen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK

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