The Effect of Dialysate Sodium on Endothelial Injury and Microcirculatory Dysfunction

Key Points The manipulation of dialysate sodium in an animal hemodialysis model has allowed for assessment of endothelial damage. Hemodialysis results in direct acute endothelial injury and microcirculatory disturbance. Hemodialysis-induced effects are aggravated with exposure to high sodium dialysate, potentially resulting in sustained injury to the glycocalyx. Background Hemodialysis causes injury to the glycocalyx, inducing shedding of syndecan-1. This damage results from hemodynamic stress of hemodialysis and injury caused by oncotic shifts in the presence of additional sodium. The aim of this study was to investigate the effects of sodium dialysate concentration on endothelial cell injury and microcirculatory dysfunction during hemodialysis. We hypothesize that changes in plasma sodium concentration will result in direct injury to the glycocalyx and reduce microcirculatory perfusion. Methods Twenty-seven healthy male Wistar Kyoto rats underwent hemodialysis: Eight were exposed to 140 mM sodium dialysate concentration (control), ten were exposed to low sodium dialysate (130 mM), and nine were exposed to high sodium dialysate (150 mM). Throughout hemodialysis, intravital microscopy was used to image the microvasculature perfusion at baseline, during extracorporeal circulation with no dialysate flow (sham), at 1 hour into hemodialysis, at 2 hours into hemodialysis, and after hemodialysis (final). Blood samples were collected at the same time points corresponding to the intravital microscopy image acquisitions to measure syndecan-1. Results The findings demonstrate a gradual increase in syndecan-1 concentration in blood plasma and a consistent trend of lower perfusion throughout the duration of the experiment in all experimental groups. Particularly, syndecan-1 concentration in plasma was significantly higher at 2 hours into hemodialysis in the high sodium dialysate group compared with the control and low sodium dialysate group. Conclusions Hemodialysis results in direct acute endothelial injury and microcirculatory disturbance. This effect is aggravated by exposure to supraphysiological concentrations of sodium, potentially resulting in sustained injury to the glycocalyx.

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Publication Details

Journal
Kidney360
Published
2025-10-03
DOI
https://doi.org/10.34067/kid.0000000949
Citations
2
Primary Topic
Dialysis and Renal Disease Management
Type
article
Field-Weighted Citation Impact
2.86
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article

The Effect of Dialysate Sodium on Endothelial Injury and Microcirculatory Dysfunction

Eric K. Patterson, G. Janssen, Christopher W. McIntyre, Lisa Hur et al.
2 citations
Kidney360
Dialysis and Renal Disease Management
2.86
article

The Effect of Dialysate Sodium on Endothelial Injury and Microcirculatory Dysfunction

Eric K. Patterson, G. Janssen, Christopher W. McIntyre, Lisa Hur, Alireza Akbari, Yanmin Zhang
article en
2 citations

Abstract

Key Points The manipulation of dialysate sodium in an animal hemodialysis model has allowed for assessment of endothelial damage. Hemodialysis results in direct acute endothelial injury and microcirculatory disturbance. Hemodialysis-induced effects are aggravated with exposure to high sodium dialysate, potentially resulting in sustained injury to the glycocalyx. Background Hemodialysis causes injury to the glycocalyx, inducing shedding of syndecan-1. This damage results from hemodynamic stress of hemodialysis and injury caused by oncotic shifts in the presence of additional sodium. The aim of this study was to investigate the effects of sodium dialysate concentration on endothelial cell injury and microcirculatory dysfunction during hemodialysis. We hypothesize that changes in plasma sodium concentration will result in direct injury to the glycocalyx and reduce microcirculatory perfusion. Methods Twenty-seven healthy male Wistar Kyoto rats underwent hemodialysis: Eight were exposed to 140 mM sodium dialysate concentration (control), ten were exposed to low sodium dialysate (130 mM), and nine were exposed to high sodium dialysate (150 mM). Throughout hemodialysis, intravital microscopy was used to image the microvasculature perfusion at baseline, during extracorporeal circulation with no dialysate flow (sham), at 1 hour into hemodialysis, at 2 hours into hemodialysis, and after hemodialysis (final). Blood samples were collected at the same time points corresponding to the intravital microscopy image acquisitions to measure syndecan-1. Results The findings demonstrate a gradual increase in syndecan-1 concentration in blood plasma and a consistent trend of lower perfusion throughout the duration of the experiment in all experimental groups. Particularly, syndecan-1 concentration in plasma was significantly higher at 2 hours into hemodialysis in the high sodium dialysate group compared with the control and low sodium dialysate group. Conclusions Hemodialysis results in direct acute endothelial injury and microcirculatory disturbance. This effect is aggravated by exposure to supraphysiological concentrations of sodium, potentially resulting in sustained injury to the glycocalyx.

Kidney360Vol. 6(11)
Western University (CA), Lawson Health Research Institute (CA), London Health Sciences Centre (CA)
Openalex Percentile: Top 8%
Dialysis and Renal Disease Management
2.86
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