Kidney Week

Abstract: SA-PO906

Online Hemodiafiltration Inhibits Endothelial Dysfunction and Vascular Calcification of Uremic Patients Modulating miR-223 Expression in Plasma Extracellular Vesicles

Session Information

• Dialysis: Cardiovascular, BP, Volume
  October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

• 701 Dialysis: Hemodialysis and Frequent Dialysis

Authors

• Marengo, Marita, Nephrology and Dialysis Unit, ASLCN1, Cuneo, Italy

Marita Marengo,

• Migliori, Massimiliano, Asl Toscana Nordovest, Camaiore, Italy

Massimiliano Migliori,

• Panichi, Vincenzo, ASl Toscana Nordovest, Camaiore, Italy

Vincenzo Panichi,

• Dellepiane, Sergio, Icahn School of Medicine at Mount Sinai, New York, New York, United States

Sergio Dellepiane,

• Cantaluppi, Vincenzo, University of Piemonte Orientale (UPO), Novara, Italy

Vincenzo Cantaluppi,

Background

Decreased inflammation and cardiovascular mortality is evident in patients with end stage chronic kidney disease (CKD) treated by on-line hemodiafiltration (OL-HDF). Extracellular vesicles (EV) are key mediators of cell-to-cell communication. This study investigated whether OL-HDF may modulate the concentration and the RNA content of plasma EV.

Methods

30 bicarbonate hemodialysis (BHD) patients were randomized 1:1 to continue BHD or switch to OL-HDF. Concentration, size, and microRNA content of plasma EV were evaluated for 9 months; we also studied EV effects on inflammation, angiogenesis and apoptosis of human endothelial cells (EC), and on osteoblast mineralization of vascular smooth muscle cells (VSMC).

Results

OL-HDF reduced different inflammatory markers such as CRP, IL6 and NGAL. All hemodialysis patients showed higher plasma levels of endothelial derived EV than healthy subjects, with no differences between BHD and OL-HDF. However, BHD-derived EV had an increased expression of the pro-atherogenic miR-223 in respect to healthy subjects or OL-HDF. Compared to EV from healthy subjects, those from hemodialysis patients reduced angiogenesis, increased EC apoptosis and VSMC calcification; however, all these detrimental effects were reduced with OL-HDF in respect to BHD. Cell transfection with miR-223 mimic or antagomiR proved the role of this miRNA in EV-induced EC and VSMC dysfunction.

Conclusion

Switch from BHD to OL-HDF significantly reduced systemic inflammation and miR-223 expression in plasma-EV, thus improving EC angiogenesis and reducing VSMC calcification.