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Abstract: TH-PO757

Extracellular Vesicles as Novel Markers in Hemodialysis Access Complications

Session Information

Category: Dialysis

  • 603 Hemodialysis: Vascular Access


  • Chopra, Tushar, None, Nashville, Tennessee, United States
  • La salvia, Sabrina, University of Virginia, Charlottesville,, West Virginia, United States
  • Musante, Luca, University of Virginia, Charlottesville,, West Virginia, United States
  • Kalantari, Kambiz, University of Virginia, Charlottesville,, West Virginia, United States
  • Intagliata, Nicolas, University of Virginia, Charlottesville,, West Virginia, United States
  • Le, Thu H., None, Nashville, Tennessee, United States
  • Erdbruegger, Uta, University of Virginia Health System, Charlottesville, Virginia, United States

Failure of hemodialysis vascular access (HVA) is the most common cause of hospitalization and morbidity among end stage renal disease (ESRD) patients. Circulating extracellular vesicles (EVs) are potential candidate biomarkers to identify patients at risk for these HVA complications and failure. We hypothesize that these circulating EVs reflect endothelial damage in patients with vascular access complications, are pro-coagulant and predict VA longterm outcome.


EVs were isolated from platelet free plasma from citrated blood of 19 patients with recurrent HVA complications (mean age 64, HD vintage 2.8 years) and 16 patients without (mean age 61, HD vintage 5.7 years). Enumeration and phenotyping of EVs was performed using imaging flow cytometry. CD42 positive, CD31, S-Endoglin (CD105), E-Selectin (CD62E) and Annexin V (AnV) positive EVs were used as surface markers for circulating EVs. The size and concentration of EVs was measured with tunable resistive pulse sensing by qNano (Izon). A thrombin generation assay (TGA) (Stago) was performed and compared between groups. All patients were followed prospectively up to 4 years and assessed for total failure of their HVA.


Endothelial derived EVs (activated (CD62E+), and non-activated (CD105+)) were significantly higher in patients with vascular access stenosis and thrombosis (CD62E: median 141,596/μl plasma, CD105: 114,983/μl plasma) compared to patients without VA complications (CD62E: median 63411/μl plasma, CD105 86505/μl plasma, CD62E p=0.014, CD105 p=0.004).
Out of the 35 patients 19 (80%) had a functioning graft at time of follow up. Higher CD31+/CD41- EV levels correlated with a functioning access up to 5 years (CD31+/CD41- EVs: functioning 406,514/μl plasma, failed 161,000/μl plasma, p=0.02). However, EV concentration, EV size profile and endogenous thrombin potential were not statistically different between patients with and without HVA complications.


Activated and non-activated endothelial derived EVs are elevated in HD patients with vascular access complications, independent of HD vintage. These EVs might reflect endothelial pathology in HVA and have the potential to guide surveillance and treatment. A larger cohort of patients needs to be examined to confirm this finding.


  • Other NIH Support