Effect of continuous hemodiafiltration (CHDF) on vascular endothelial cell function in sepsis patients

Objectives

To remove humoral mediators in sepsis patients, continuous hemodiafiltration (CHDF) was performed and its effect on vascular endothelial cell function was examined.

Subjects and methods

The study subjects were 10 patients with sepsis who received CHDF for more than 3 days at our facility. A PMMA membrane was used as a hemofilter, and nafamostat mesylate was administered as an anticoagulant. Measurements were performed before CHDF and 30 min and 24, 48 and 72 hours after CHDF, of granulocytic elastase, PAI-I, IL-6, IL-1ra, ELAM-1, endothelin-1, and NOx. The survival group (six cases) and nonsurvival group (four cases) were separated according to the outcome at 2 weeks after CHDF and were separately analyzed.

Results

Before CHDF treatment, granulocytic elastase, PAI-I and NOx were significantly higher in the survival group than in the nonsurvival group. Starting 48 hours after CHDF, granulocytic elastase decreased significantly in the survival group and increased significantly in the nonsurvival group. PAI-I was significantly lower 24 and more hours after CHDF in the survivors, whereas it rather increased in the nonsurvivors. In both groups, IL-6, IL-1ra and NOx were significantly decreased by CHDF. ELAM-1 and endothelin-1 appeared to decrease in both groups, although there was no statistical significance. There was no significant difference in BNP between the groups.

Discussion

PAI-I, which is associated with activation of vascular endothelial cells, and granulocytic elastase, which is associated with neutrophil activation, were significantly higher in the survival group before CHDF. After CHDF, they significantly decreased in the survival group and rather increased in the nonsurvival group. These data suggest that vascular endothelial cell damage was suppressed by CHDF in the survival group. In the nonsurvival group, cytokines decreased while granulocytic elastase and PAI-I did not decrease, suggesting that it is more important to control vascular endothelial damage in sepsis patients. The NO metabolite NOx, a vascular endothelial relaxation factor, endothelin-1, a contraction factor, and ELAM-1, an adhesion factor, decreased during CHDF, but showed no difference between the two groups of patients.

Conclusion

The results suggest the possibility that CHDF suppresses vascular endothelial cell damage in sepsis patients.