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Article: Inflammation in peritoneal dialysis

TitleInflammation in peritoneal dialysis
Authors
KeywordsAdipocytes
Fibrosis
Inflammation
Mesothelium
Peritoneal dialysis
Issue Date2010
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEC
Citation
Nephron - Clinical Practice, 2010, v. 116 n. 1, p. c11-c18 How to Cite?
AbstractDuring peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiological hypertonic environment with high glucose content and low pH. Current sterile dialysis solutions cause inflammation in the submesothelial compact zone that leads to fibrosis, neoangiogenesis, progressive increases in solute transfer and even ultrafiltration failure. The peritoneal dysfunction will further be amplified with the development of an epithelial-to-mesenchymal transition of mesothelial cells and the dissipation of the osmotic driving force through increased area and solute transport that accompanied neoangiogenesis of the submesothelial microvasculature. The alteration in the peritoneal membrane will further be aggravated by peritonitis, advanced glycation end-products and glucose degradation products. Finally, there are emerging new data supporting a pro-inflammatory role of peritoneal adipocytes. © 2010 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/163314
ISSN
2015 Impact Factor: 1.471
2015 SCImago Journal Rankings: 0.658
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLeung, JCKen_HK
dc.date.accessioned2012-09-05T05:29:58Z-
dc.date.available2012-09-05T05:29:58Z-
dc.date.issued2010en_HK
dc.identifier.citationNephron - Clinical Practice, 2010, v. 116 n. 1, p. c11-c18en_HK
dc.identifier.issn1660-2110en_HK
dc.identifier.urihttp://hdl.handle.net/10722/163314-
dc.description.abstractDuring peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiological hypertonic environment with high glucose content and low pH. Current sterile dialysis solutions cause inflammation in the submesothelial compact zone that leads to fibrosis, neoangiogenesis, progressive increases in solute transfer and even ultrafiltration failure. The peritoneal dysfunction will further be amplified with the development of an epithelial-to-mesenchymal transition of mesothelial cells and the dissipation of the osmotic driving force through increased area and solute transport that accompanied neoangiogenesis of the submesothelial microvasculature. The alteration in the peritoneal membrane will further be aggravated by peritonitis, advanced glycation end-products and glucose degradation products. Finally, there are emerging new data supporting a pro-inflammatory role of peritoneal adipocytes. © 2010 S. Karger AG, Basel.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NECen_HK
dc.relation.ispartofNephron - Clinical Practiceen_HK
dc.subjectAdipocytesen_HK
dc.subjectFibrosisen_HK
dc.subjectInflammationen_HK
dc.subjectMesotheliumen_HK
dc.subjectPeritoneal dialysisen_HK
dc.subject.meshAdipocytes - Pathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshHumansen_US
dc.subject.meshInflammation - Pathology - Prevention & Control - Therapyen_US
dc.subject.meshPeritoneal Dialysis - Adverse Effects - Methodsen_US
dc.subject.meshPeritonitis - Etiology - Pathology - Therapyen_US
dc.titleInflammation in peritoneal dialysisen_HK
dc.typeArticleen_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_OA_fulltexten_US
dc.identifier.doi10.1159/000314544en_HK
dc.identifier.pmid20460934-
dc.identifier.scopuseid_2-s2.0-77951946920en_HK
dc.identifier.hkuros180804-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77951946920&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume116en_HK
dc.identifier.issue1en_HK
dc.identifier.spagec11en_HK
dc.identifier.epagec18en_HK
dc.identifier.isiWOS:000280870700003-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK

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