Of veins, valves, and vascular access!

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Presentation transcript:

Of veins, valves, and vascular access! Prabir Roy-Chaudhury, Jenq-Shyong Chan, Timmy Lee, Meenakshi Mistry, Begoña Campos, Yang Wang, Rino Munda Kidney International Volume 82, Issue 11, Pages 1236-1237 (December 2012) DOI: 10.1038/ki.2012.316 Copyright © 2012 International Society of Nephrology Terms and Conditions

Figure 1 Venous valves. A stenotic venous segment from a patient with a dysfunctional arteriovenous (AV) access who underwent a revision procedure. Note the prominent venous valves (thin black arrows) that have fused together in the middle of the vein (asterisk), which could predispose to non-laminar flow and altered hemodynamic shear stress profiles; resulting in neointimal hyperplasia and venous stenosis. Note also the beginnings of hypertrophy in some areas of the valve (broad red arrow). H and E, hematoxylin and eosin. Kidney International 2012 82, 1236-1237DOI: (10.1038/ki.2012.316) Copyright © 2012 International Society of Nephrology Terms and Conditions

Figure 2 Cellular phenotyping of venous valves. (a) A low-power view of a venous valve stained with α-smooth muscle actin (SMA, × 100), 7 days after creation of an arteriovenous (AV) fistula in our pig model of AV fistula stenosis. (b–f) High-power views of the cellular phenotypes present within venous valves (from the box region in (a). Note that the majority of cells are smooth muscle actin +ve (b), vimentin +ve (c), and desmin -ve (d) myofibroblasts. Note also the presence of cellular proliferation (e) and macrophages (f) within the venous valve. PCNA, proliferating cell nuclear antigen. Kidney International 2012 82, 1236-1237DOI: (10.1038/ki.2012.316) Copyright © 2012 International Society of Nephrology Terms and Conditions