Kidney Week

Abstract: TH-PO0457

Extracellular Vesicles: Promising Biomarkers for Dialysis-Induced Organ Injury

Session Information

• Hemodialysis: Novel Markers and Case Reports
  November 06, 2025 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

• 801 Dialysis: Hemodialysis and Frequent Dialysis

Authors

• Chaara, Sabrine, Amsterdam UMC Locatie VUmc, Amsterdam, NH, Netherlands

Sabrine Chaara, MD

• Nube, Menso, Amsterdam UMC Locatie VUmc, Amsterdam, NH, Netherlands

Menso Nube, MD, PhD

• de Roij van Zuijdewijn, Camiel LM, Amsterdam UMC Locatie VUmc, Amsterdam, NH, Netherlands

Camiel LM de Roij van Zuijdewijn, MD, PhD

• Nieuwland, Rienk, Amsterdam UMC Locatie AMC, Amsterdam, NH, Netherlands

Rienk Nieuwland

• Grooteman, Muriel P., Amsterdam UMC Locatie VUmc, Amsterdam, NH, Netherlands

Muriel P. Grooteman, MD, PhD

Background

While hemodialysis (HD) is a life-sustaining treatment, the procedure itself has been associated with adverse effects, such as bio-incompatibility (BI) issues and cardiovascular (CV) tissue injury. Extracellular vesicles (EVs), which are released during HD by activated circulating blood cells and CV tissues, may serve as biomarkers of cellular damage. Whereas cardiac enzymes, such as troponins, are small molecules which can be removed by convective transport, EVs are too large for transmembrane passage. In this exploratory study, we assessed the kinetics of both EV-types to determine the timing and origin of their release.

Methods

Six chronic HD patients were included. Blood samples were collected at 3 sampling points: S1: arterial line (before pump), S2: between pump and dialyzer, and S3 venous line (after dialyzer). Plasma concentrations of CV-derived (CD144+,Connexin-43+) and BI-derived (CD45+,CD61+,CD235a⁺) EVs were measured by flow cytometry at t₀,t₃₀,t₆₀,t₁₈₀ and t₂₄₀ at all sites. Data were corrected for hemoconcentration.

Results

CV-derived EVs (figure 1): From t₁₂₀ onwards, both Connexin-43+ (myocardium- and endothelium-derived) and CD144+ (endothelium-derived) EVs showed a steep increase in the arterial line (outside the ECC, p<0.001). Within the ECC, however, changes were not observed.
BI-derived EVs (figure 2): leukocyte- (CD45+), platelet- (CD61+) and erythrocyte-derived (CD235a⁺) EVs remained stable in the arterial line (outside the ECC) during treatment. Within the ECC (S1-S3), however, CD45+EVs increased significantly at t₃₀,t₁₂₀ and t₁₈₀, and CD61+EVs at t₃₀ and t₂₄₀. CD235+EVs increased within the ECC during the last part of HD.

Conclusion

1) CV-derived EVs originate outside the ECC and exhibit a steep rise in the second part of the sessions.
2) BI-derived EVs originate within the ECC, mainly early and remain elevated thereafter.

Digital Object Identifier (DOI)

• doi: 10.1681/ASN.20258sqgfe01