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Genetic Causation of Neointimal Hyperplasia in Hemodialysis Vascular Access Dysfunction

Authors

  • Timmy Lee,

    1. Department of Internal Medicine, Division of Nephrology and Hypertension, University of Cincinnati, Cincinnati, Ohio
    2. Cincinnati Veterans Administration Medical Center, Cincinnati, Ohio
    3. Dialysis Access Program, University of Cincinnati, Cincinnati, Ohio
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  • Davinder Wadehra

    1. Department of Internal Medicine, Division of Nephrology and Hypertension, University of Cincinnati, Cincinnati, Ohio
    2. Dialysis Access Program, University of Cincinnati, Cincinnati, Ohio
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Address correspondence to: Timmy Lee, MD, MSPH, FACP, FASN, Assistant Professor of Clinical Medicine, Department of Internal Medicine, Division of Nephrology and Hypertension, University of Cincinnati, 231 Albert Sabin Way, M.L.0585, Cincinnati, OH 45267-0585, Tel.: 513-558-4782, Fax: 513-558-4309, or e-mail: timmy.lee@uc.edu.

Abstract

The major cause of hemodialysis vascular access failure is venous stenosis resulting from neointimal hyperplasia. Genetic factors have been shown to be associated with cardiovascular disease and peripheral vascular disease (PVD) in the general population. Genetic factors may also play an important role in vascular access stenosis and development of neointimal hyperplasia by affecting pathways that lead to inflammation, endothelial function, oxidative stress, and vascular smooth muscle proliferation. This review will discuss the role of genetics in understanding neointimal hyperplasia development in hemodialysis vascular access dysfunction and other disease processes with similar neointimal hyperplasia development such as coronary artery disease and PVD.

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