Portions of this work were presented in abstract form at the Vascular Access Society Meeting, Istanbul, Turkey, May 2011 and American Society of Nephrology Renal Week, Philadelphia, PA, November 2011.
American Society of Diagnostic and Interventional Nephrology
Comparative Analysis of Cellular Phenotypes Within the Neointima From Vein Segments Collected Prior to Vascular Access Surgery and Stenotic Arteriovenous Dialysis Accesses
Article first published online: 17 DEC 2013
© 2013 Wiley Periodicals, Inc.
Seminars in Dialysis
Volume 27, Issue 3, pages 303–309, May–June 2014
How to Cite
Lee, T., Wang, Y., Arend, L., Cornea, V., Campos, B., Munda, R. and Roy-Chaudhury, P. (2014), Comparative Analysis of Cellular Phenotypes Within the Neointima From Vein Segments Collected Prior to Vascular Access Surgery and Stenotic Arteriovenous Dialysis Accesses. Seminars in Dialysis, 27: 303–309. doi: 10.1111/sdi.12172
- Issue published online: 24 APR 2014
- Article first published online: 17 DEC 2013
- NIH. Grant Numbers: 5K23DK083528-04, 5U01-DK82218, 5U01-DK82218S, 5R01-EB004527, 1R21-DK089280-01
- NIH/NCCR. Grant Number: UL1RR026314
Venous stenosis, secondary to venous neointimal hyperplasia (VNH), at the arteriovenous anastomosis (AV) is a major etiology of vascular access failure in AV fistulas (AVF) and AV grafts (AVG). Recently, our group has reported that severe VNH also occurs prior to vascular access placement. The objective of this study was to perform a comparison of the cellular phenotypes within the neointima from veins collected from subjects at the time of new vascular access creation and stenotic veins from subjects with failed AVGs and AVFs. Vein samples, collected at the time of new access surgery, and stenotic vein segments, collected at access revision, were evaluated for expression of α-smooth muscle actin (SMA), vimentin, and desmin within the neointima, and quantified using semiquantitative scoring. Within the neointima, the majority of cells from vein samples collected at the time of new access surgery were contractile smooth muscle cells, and veins from stenotic AVF and AVG were predominately myofibroblasts. Our results suggest the possibility of different mechanistic pathways in response to vascular injury that occurs prior to vascular access creation vs. after access creation, and that divergent therapeutic approaches may be needed for treating vascular injury in these two settings.