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Article: Preventing peritoneal fibrosis - Insights from the laboratory

TitlePreventing peritoneal fibrosis - Insights from the laboratory
Authors
Issue Date2003
PublisherMultimed, Inc. The Journal's web site is located at http://pdiconnect.com
Citation
Peritoneal Dialysis International, 2003, v. 23 SUPPL. 2, p. S37-S41 How to Cite?
Abstract◆ Objective: Peritoneal fibrosis is one of the most serious complications of peritoneal dialysis (PD). Peritoneal fibrosis is characterized by activation of the peritoneal resident cells, accumulation and deposition of excess matrix proteins within the interstitium, and neoangiogenesis and vasculopathy of the peritoneal microvasculature. Compelling evidence now exists to show that elevated glucose concentrations present as the osmotic agent in PD solutions are, per se, responsible for those detrimental changes. Until alternative osmotic agents can fully replace glucose in PD solutions, novel therapeutic strategies are essential to preserve the structural and functional properties of the peritoneum. This review highlights recent experimental data that may offer potential strategies for preservation of the peritoneal structure and improvement of clinical outcome. ◆ Method: Literature review. ◆ Results: Compelling evidence now exists to show that the bioincompatible nature of PD solutions - in particular, elevated glucose concentrations and glucose byproducts - play a pivotal role in the initiation of peritoneal fibrosis. Animal and in vitro studies provide some insight into methods that can potentially be employed to alleviate or retard peritoneal fibrosis. Those methods include use of alterative osmotic agents (polyglucose or amino acids), administration of TGFβ1 antagonists, gene therapy, and pharmacologic interventions. ◆ Conclusions: Knowledge of the pathogenesis of peritoneal fibrosis has allowed independent researchers to design therapeutic strategies that abrogate excess matrix synthesis and deposition in cultured peritoneal cells and in animal models of experimental peritoneal fibrosis alike. Encouraging results have been obtained in those studies, but it remains to be determined whether the studied strategies can alleviate clinical disease. Future studies will enable us to establish specific molecules that can be targeted clinically to restrict the progressive deterioration of the peritoneal membrane as a biologic dialyzing organ.
Persistent Identifierhttp://hdl.handle.net/10722/162741
ISSN
2015 Impact Factor: 1.298
2015 SCImago Journal Rankings: 0.683
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYung, Sen_US
dc.contributor.authorChan, TMen_US
dc.date.accessioned2012-09-05T05:22:59Z-
dc.date.available2012-09-05T05:22:59Z-
dc.date.issued2003en_US
dc.identifier.citationPeritoneal Dialysis International, 2003, v. 23 SUPPL. 2, p. S37-S41en_US
dc.identifier.issn0896-8608en_US
dc.identifier.urihttp://hdl.handle.net/10722/162741-
dc.description.abstract◆ Objective: Peritoneal fibrosis is one of the most serious complications of peritoneal dialysis (PD). Peritoneal fibrosis is characterized by activation of the peritoneal resident cells, accumulation and deposition of excess matrix proteins within the interstitium, and neoangiogenesis and vasculopathy of the peritoneal microvasculature. Compelling evidence now exists to show that elevated glucose concentrations present as the osmotic agent in PD solutions are, per se, responsible for those detrimental changes. Until alternative osmotic agents can fully replace glucose in PD solutions, novel therapeutic strategies are essential to preserve the structural and functional properties of the peritoneum. This review highlights recent experimental data that may offer potential strategies for preservation of the peritoneal structure and improvement of clinical outcome. ◆ Method: Literature review. ◆ Results: Compelling evidence now exists to show that the bioincompatible nature of PD solutions - in particular, elevated glucose concentrations and glucose byproducts - play a pivotal role in the initiation of peritoneal fibrosis. Animal and in vitro studies provide some insight into methods that can potentially be employed to alleviate or retard peritoneal fibrosis. Those methods include use of alterative osmotic agents (polyglucose or amino acids), administration of TGFβ1 antagonists, gene therapy, and pharmacologic interventions. ◆ Conclusions: Knowledge of the pathogenesis of peritoneal fibrosis has allowed independent researchers to design therapeutic strategies that abrogate excess matrix synthesis and deposition in cultured peritoneal cells and in animal models of experimental peritoneal fibrosis alike. Encouraging results have been obtained in those studies, but it remains to be determined whether the studied strategies can alleviate clinical disease. Future studies will enable us to establish specific molecules that can be targeted clinically to restrict the progressive deterioration of the peritoneal membrane as a biologic dialyzing organ.en_US
dc.languageengen_US
dc.publisherMultimed, Inc. The Journal's web site is located at http://pdiconnect.comen_US
dc.relation.ispartofPeritoneal Dialysis Internationalen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshHumansen_US
dc.subject.meshPeritoneal Fibrosis - Etiology - Prevention & Controlen_US
dc.titlePreventing peritoneal fibrosis - Insights from the laboratoryen_US
dc.typeArticleen_US
dc.identifier.emailYung, S:ssyyung@hku.hken_US
dc.identifier.emailChan, TM:dtmchan@hku.hken_US
dc.identifier.authorityYung, S=rp00455en_US
dc.identifier.authorityChan, TM=rp00394en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid17986555-
dc.identifier.scopuseid_2-s2.0-0345874657en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0345874657&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume23en_US
dc.identifier.issueSUPPL. 2en_US
dc.identifier.spageS37en_US
dc.identifier.epageS41en_US
dc.identifier.isiWOS:000188533200008-
dc.publisher.placeCanadaen_US
dc.identifier.scopusauthoridYung, S=22636568800en_US
dc.identifier.scopusauthoridChan, TM=7402687700en_US

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