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Kidney Week

Abstract: TH-PO206

Rise of Plasma Sodium Levels Is Followed by an Increase of Plasma Syndecan 1 in Hemodialysis Patients

Session Information

Category: Dialysis

  • 701 Dialysis: Hemodialysis and Frequent Dialysis


  • Koch, Josephine, University Medical Center Groningen, Groningen, Groningen, Netherlands
  • Idzerda, Nienke, University Medical Center Groningen, Groningen, Netherlands
  • Ettema, Esmee, University Medical Center Groningen, Groningen, Netherlands
  • Dam, Wendy, University Medical Center Groningen, Groningen, Netherlands
  • Franssen, Casper F.M., University Medical Center Groningen, Groningen, Groningen, Netherlands
  • van den Born, Jacob, University Medical Center Groningen, Groningen, Netherlands

In hemodialysis (HD) patients, endothelial dysfunction (ED) contributes to atherosclerosis. A major hallmark of ED is loss of glycocalyx evidenced by shedding of syndecan-1 into the blood stream. Release of syndecan-1 is seen in pro-inflammatory and pro-oxidative conditions such as in HD patients. HD by the Hemocontrol biofeedback system (HHD) is characterized by initially higher dialysate and plasma sodium levels. Using HHD as a model for an acute increase in plasma sodium, we investigated associations between courses of plasma sodium and syndecan-1 during HHD and standard HD (SHD).


Plasma syndecan-1 was measured by ELISA in blood samples obtained from a cohort of 29 prevalent HD patients before, during and after HHD and SHD (randomized sequence). Wilcoxon signed-rank test or paired student’s t-test was used to compare syndecan-1 levels between SHD and HHD. Intradialytic shedding of syndecan-1 was determined by area under the curve analyses. Associations with the intradialytic course of syndecan-1 were analyzed with a mixed effects repeated-measures model.


During HHD, plasma sodium increased early after the start of HD (predialysis 139,1 mmol/L; at 30 minutes of HD 142.3 mmol/L; P<0.0001) whereas sodium did not increase significantly during SHD. During HHD, plasma syndecan-1 increased after 120 minutes of HD (P=0.007). Plasma syndecan-1 also increased significantly during SHD (within 120 minutes; P=0.003) but at 120 minutes, the rise in syndecan-1 levels was significantly higher in HHD as compared to SHD (+42.9% vs. +17.2%; P=0.021). The total amount of shed syndecan-1 was higher during HHD than during SHD, albeit at borderline significance (P=0.05). Lower plasma sodium and osmolality before dialysis were independent predictors of syndecan-1 increase during dialysis (P=0.001 for both groups). In HHD, a higher cumulative UF volume was independently associated with more intradialytic syndecan-1 shedding (P=0.001).


Plasma syndecan-1 levels increased significantly during both HHD and SHD. In HHD, this rise was significantly greater and occurred earlier as compared to SHD. This may reflect ED resulting from increased sodium load. Further research to assess long term effects and clinical implications of high salt exposure is needed.