ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: PO1825

Effect of Uremia on Endothelial Cell Damage Is Mediated by Excessive Neutrophil Extracellular Trap Formation

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms


  • Kim, Jwa-kyung, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
  • Lee, Hoi Woul, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
  • Kim, Sung gyun, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)

Uremia is a clinical syndrome characterized by accumulation of various uremic toxins and associated metabolic abnormalities in chronic kidney disease (CKD). Patients with CKD are at increased risk for cardiovascular (CV) disease and death, and endothelial dysfunction may be a key uremia-specific risk factor. However, the mechanism by which uremia influences endothelial dysfunction is still unclear. We report a role for excessive neutrophil extracellular trap (NET) formation induced by uremic serum on endothelial cell (EC) injury.


Plasma nucleosome and myeloperoxidase-DNA, representative markers of in vivo NETs, and the intracellular adhesion molecule (ICAM)-1 level were measured in incident hemodialysis (HD) patients and healthy volunteer (HV), and their prognostic role was evaluated. For in vitro study, we differentiated HL-60 cells into neutrophil-like cells (dHL-60) by applying retinoic acid, and the effect of uremic serum on dHL-60 and ECs were determined.


The amount of in vivo NETs were significantly higher in incident HD patients compared to HV, and the markers were strongly associated with ICAM-1 levels. In particular, nucleosome and ICAM-1 levels were independent predictors of a composite endpoint, all-cause mortality or vascular access failure. In vitro, uremic serum derived from HD patients showed significantly increased NETs formation from dHL-60, and these NETs significantly decreased EC viability and induced apoptosis. In addition, the ICAM-1 level in HUVEC supernatant was significantly increased by uremic serum-induced NETs compared to control serum-induced NETs.


Dysregulated neutrophil activities in the uremic milieu may play a key role in endothelial damage and vascular inflammatory responses.