New Insights into the Pathogenesis of Intradialytic Hypertension
Joelle Hajal1, Youakim Saliba1, Najat Joubran2, Ghassan Sleilaty3, Dima Chacra3, Shafika Assaad4, Dania Chelala3, #, Nassim Farès1, *, #
Identifiers and Pagination:Year: 2018
First Page: 87
Last Page: 99
Publisher Id: TOUNJ-11-87
Article History:Received Date: 22/8/2018
Revision Received Date: 28/11/2018
Acceptance Date: 6/12/2018
Electronic publication date: 31/12/2018
Collection year: 2018
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Intradialytic hypertension is identified as an independent predictor of adverse clinical outcome in hemodialysis patients. Little is known about its pathophysiological mechanism.
The aim of this study is to provide new insights into the mechanisms underlying this arterial pressure dysregulation.
62 subjects on chronic hemodialysis were included in this study. Blood pressure was monitored before, during and following each dialysis session for a 3-month period. Pre- and post-dialysis blood samples were drawn from all the subjects to perform immunoassays, monocyte extractions and western blot analyses.
Blood pressure values separated the subjects with in two groups: normal blood pressure (n=53) and intradialytic hypertension (n=9) groups. Renin, angiotensin converting enzyme I and aldosterone plasma concentrations significantly diverged between the groups. Vascular endothelial nitric oxide assessment revealed significantly lower plasma L-citrulline and angiotensin-converting enzyme II in post-dialysis intradialytic hypertensive patients, along with high endothelin I and asymmetric dimethylarginine concentrations. Plasma collectrin levels were significantly higher in pre and post-dialysis intradialytic hypertensive group compared to a normal blood pressure group. Post-dialysis interleukin 6 was significantly higher in intradialytic hypertensive group compared to normal blood pressure group. Finally, pre-dialysis intradialytic hypertension was associated with significantly higher circulating vascular endothelial growth factor C with monocytic up-regulation of vascular endothelial growth factor C/tonicity-responsive enhancer binding protein expression.
Impairment of vascular endothelial nitric oxide key regulatory elements, as well as monocytic vascular endothelial growth factor C seems to be more prevalent in intradialytic hypertension. These clues could pinpoint novel therapeutic interventions in intradialytic hypertension management.