Kidney Week

Abstract: SA-PO447

Sodium-Induced Microcirculatory Dysfunction During Hemodialysis

Session Information

• Hemodialysis and Frequent Dialysis: Clearance, Technology, Infection
  November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
  Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

• 701 Dialysis: Hemodialysis and Frequent Dialysis

Authors

• Hur, Lisa, Western University, London, Ontario, Canada

Lisa Hur,

• Zhang, Yanmin, Western University, London, Ontario, Canada

Yanmin Zhang,

• Janssen, Barry, Western University, London, Ontario, Canada

Barry Janssen,

• McIntyre, Christopher W., London Health Sciences Centre London Kidney Clinical Research Unit, London, Ontario, Canada

Christopher W. McIntyre,

Background

Hemodialysis (HD) results in microcirculatory dysfunction (MD) leading to recurrent cardiac ischemia. Endothelial glycocalyx is vulnerable to circulatory and oncotic stress (predominantly Na⁺ mediated)- inducing shedding of syndecan-1 (syn1), a transmembrane heparan sulfate proteoglycan. The glycocalyx binds Na⁺, buffering sudden serum Na⁺ shifts, and can be damaged with acute changes in Na⁺ concentration ([Na⁺ ]). The aim of this study is to investigate the effects of [Na⁺ ] dialysate on endothelial cell injury and MD during HD. We hypothesize that avoidance of higher [Na⁺ ] dialysate would have a direct protective effect on the endothelial glyocalyx and minimize directly observed HD-associated microcirculatory disturbance.

Methods

8 healthy male Wistar Kyoto rats underwent HD: 4 were exposed to a higher dialysate [Na⁺ ] (140mM) and 4 were exposed to dialysate [Na⁺ ] below typical rat plasma Na⁺ level (hyponatremic-130mM). Throughout HD, intravital microscopy (IVM) was used to image skeletal muscle microvasculature at baseline, during extracorporeal circulation with no dialysate flow (“Sham”), at 1 hr into HD, at 2 hrs into HD, and post HD (“Final”). The IVM images were processed to automatically derive the number of identified intersecting points, to quantify microcirculatory blood flow and observe the change in perfusion index at each timepoint. Blood samples were collected at the same timepoints corresponding to the IVM image acquisitions to measure syn1 and quantify glycocalyx shedding during HD. Continuous BP recordings were made from carotid artery cannulation.

Results

BP response to HD was comparable between the two groups. We observed progressive increase in syn1 concentration in blood plasma sampled throughout the duration of the experiment in both groups (Fig 1A). The hyponatremic group demonstrated a consistent trend of lower perfusion index at all timepoints relative to the comparator group (ns, Fig 1B).

Conclusion

Preliminary data in healthy rats suggests that a single HD session results in syn1 release from the vasculature- indicating acute HD-associated endothelial injury. Limiting exposure to intradialytic Na⁺ may reduce MD under the stress of HD, despite equivalent systemic hemodynamic response.