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A fresh look into the pathophysiology of ischemia-induced complications in patients with chronic kidney disease undergoing hemodialysis

Authors Honore PM, Jacobs R, De Waele E, Van Gorp V, De Regt J, Joannes-Boyau O, Boer W, Spapen HD

Received 17 October 2014

Accepted for publication 23 January 2015

Published 13 March 2015 Volume 2015:8 Pages 25—28


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 4

Editor who approved publication: Professor Pravin Singhal

Patrick M Honore,1 Rita Jacobs,1 Elisabeth De Waele,1 Viola Van Gorp,1 Jouke De Regt,1 Olivier Joannes-Boyau,2 Willem Boer,3 Herbert D Spapen1

1Intensive Care Department, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium; 2Intensive Care Unit, Haut Leveque University Hospital of Bordeaux, University of Bordeaux 2, Pessac, France; 3Intensive Care Department, Ziekenhuis Oost Limburg, Genk, Belgium

Abstract: Recent case reports of acute esophageal necrosis in patients with chronic kidney disease (CKD) undergoing hemodialysis encouraged us to look beyond hypoperfusion/ischemia as a sole explanation for this dramatic complication. At least three intriguing pathways, ie, accumulation of protein-bound toxins, endotoxin translocation, and altered mucosal defense mechanisms, have been proposed to explain the inherent susceptibility of CKD patients to developing ischemia-related and cardiovascular events. Interestingly, all the proposed pathways can be potentially antagonized or attenuated. At present, however, it is not known whether one pathway predominates or if any interaction exists between these pathways. More solid experimental and clinical data are warranted to acquire a better insight into the complex pathogenesis of CKD-associated ischemia.

Keywords: chronic kidney disease, ischemia, pathophysiology, cardiovascular events

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