The Effect of Dialysate Sodium on Endothelial Injury and Microcirculatory Dysfunction.

Background: Hemodialysis (HD) causes injury to the glycocalyx, inducing shedding of syndecan-1. This damage results from hemodynamic stress of HD and injury caused by oncotic shifts in the presence of additional sodium. The aim of this study is to investigate the effects of sodium dialysate concentration on endothelial cell injury and microcirculatory dysfunction during HD. 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 HD: eight were exposed to 140mM sodium dialysate concentration (control), ten were exposed to low sodium dialysate (130mM), and nine were exposed to high sodium dialysate (150mM). Throughout HD, intravital microscopy was used to image the microvasculature perfusion at baseline, during extracorporeal circulation with no dialysate flow ("Sham"), at 1 hr into HD, at 2 hrs into HD, and post HD ("Final"). Blood samples were collected at the same timepoints 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 hrs into HD in the high sodium dialysate group compared to the control and low sodium dialysate group.

Conclusions: HD 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.