NFκB in the development of endothelial activation and damage in uremia: an in vitro approach.

Impaired hemostasis coexists with accelerated atherosclerosis in patients with chronic kidney disease (CKD). The elevated frequency of atherothrombotic events has been associated with endothelial dysfunction. The relative contribution of the uremic state and the impact of the renal replacement thera...

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Autores principales:	Carolina Caballo, Marta Palomo, Aleix Cases, Ana M Galán, Patricia Molina, Manel Vera, Xavier Bosch, Gines Escolar, Maribel Diaz-Ricart
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3282c02b99384f9b8007bcfe2bfa9e6b
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spelling	oai:doaj.org-article:3282c02b99384f9b8007bcfe2bfa9e6b2021-11-18T07:07:54ZNFκB in the development of endothelial activation and damage in uremia: an in vitro approach.1932-620310.1371/journal.pone.0043374https://doaj.org/article/3282c02b99384f9b8007bcfe2bfa9e6b2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22937042/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Impaired hemostasis coexists with accelerated atherosclerosis in patients with chronic kidney disease (CKD). The elevated frequency of atherothrombotic events has been associated with endothelial dysfunction. The relative contribution of the uremic state and the impact of the renal replacement therapies have been often disregarded. Plasma markers of endothelial activation and damage were evaluated in three groups of patients with CKD: under conservative treatment (predialysis), on hemodialysis, and on peritoneal dialysis. Activation of p38 MAPK and the transcription factor NFκB was assessed in endothelial cell (EC) cultures exposed to pooled sera from each group of patients. Most of the markers evaluated (VCAM-1, ICAM-1, VWF, circulating endothelial cells) were significantly higher in CDK patients than in controls, being significantly more increased in the group of peritoneal dialysis patients. These results correlated with the activation of both p38 MAPK and NFκB in EC cells exposed to the same sera samples, and also to the peritoneal dialysis fluids. Hemodialysis did not further contribute to the endothelial damage induced by the uremic state observed in predialysis patients, probably due to the improved biocompatibility of the hemodialysis technique in recent years, resulting in lower cellular activation. However, peritoneal dialysis seemed to exert a significant proinflammatory effect on the endothelium that could be related to the high glucose concentrations and glucose degradation products present in the dialysis fluid. Although peritoneal dialysis has been traditionally considered a more physiological technique, our results raise some doubts with respect to inflammation and EC damage.Carolina CaballoMarta PalomoAleix CasesAna M GalánPatricia MolinaManel VeraXavier BoschGines EscolarMaribel Diaz-RicartPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 8, p e43374 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Carolina Caballo Marta Palomo Aleix Cases Ana M Galán Patricia Molina Manel Vera Xavier Bosch Gines Escolar Maribel Diaz-Ricart NFκB in the development of endothelial activation and damage in uremia: an in vitro approach.
description	Impaired hemostasis coexists with accelerated atherosclerosis in patients with chronic kidney disease (CKD). The elevated frequency of atherothrombotic events has been associated with endothelial dysfunction. The relative contribution of the uremic state and the impact of the renal replacement therapies have been often disregarded. Plasma markers of endothelial activation and damage were evaluated in three groups of patients with CKD: under conservative treatment (predialysis), on hemodialysis, and on peritoneal dialysis. Activation of p38 MAPK and the transcription factor NFκB was assessed in endothelial cell (EC) cultures exposed to pooled sera from each group of patients. Most of the markers evaluated (VCAM-1, ICAM-1, VWF, circulating endothelial cells) were significantly higher in CDK patients than in controls, being significantly more increased in the group of peritoneal dialysis patients. These results correlated with the activation of both p38 MAPK and NFκB in EC cells exposed to the same sera samples, and also to the peritoneal dialysis fluids. Hemodialysis did not further contribute to the endothelial damage induced by the uremic state observed in predialysis patients, probably due to the improved biocompatibility of the hemodialysis technique in recent years, resulting in lower cellular activation. However, peritoneal dialysis seemed to exert a significant proinflammatory effect on the endothelium that could be related to the high glucose concentrations and glucose degradation products present in the dialysis fluid. Although peritoneal dialysis has been traditionally considered a more physiological technique, our results raise some doubts with respect to inflammation and EC damage.
format	article
author	Carolina Caballo Marta Palomo Aleix Cases Ana M Galán Patricia Molina Manel Vera Xavier Bosch Gines Escolar Maribel Diaz-Ricart
author_facet	Carolina Caballo Marta Palomo Aleix Cases Ana M Galán Patricia Molina Manel Vera Xavier Bosch Gines Escolar Maribel Diaz-Ricart
author_sort	Carolina Caballo
title	NFκB in the development of endothelial activation and damage in uremia: an in vitro approach.
title_short	NFκB in the development of endothelial activation and damage in uremia: an in vitro approach.
title_full	NFκB in the development of endothelial activation and damage in uremia: an in vitro approach.
title_fullStr	NFκB in the development of endothelial activation and damage in uremia: an in vitro approach.
title_full_unstemmed	NFκB in the development of endothelial activation and damage in uremia: an in vitro approach.
title_sort	nfκb in the development of endothelial activation and damage in uremia: an in vitro approach.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/3282c02b99384f9b8007bcfe2bfa9e6b
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NFκB in the development of endothelial activation and damage in uremia: an in vitro approach.

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