Abstract: Autologous arteriovenous fistula (AVF) is the most important route of blood access for hemodialysis, and failure of AVF may seriously limit its clinical application. Stenosis in venous outflow tract is a common cause of AVF failure, pathologically due to the neointimal hyperplasia (NIH). The mechanisms underlying NIH include a series of cascade reactions in local vessels, such as inflammation, oxidative stress and vascular remodeling, leading to vascular stenosis and AVF failure. On the other hand, hyperactive sympathetic nerve function is frequently present in end stage renal disease patients, which may also take part in the occurrence of NIH and AVF dysfunction through several pathways. This review focuses on the possible mechanisms of sympathetic activation to the development of NIH, aiming to provide a new theoretical explanation and a new intervention target for the prevention and treatment of AVF failure.

Key words: Sympathetic nerve, End stage renal disease, Arteriovenous fistula, Neointimal hyperplasia, Renal denervation