Understanding Intimal Hyperplasia Biology in Hemodialysis Access

The most common cause of hemodialysis access dysfunction is venous stenosis resulting from intimal hyperplasia. Intimal hyperplasia is a fibromuscular thickening of the vessel wall. Its occurrence is most commonly at the perianastomotic region of arteriovenous (AV) fistulas and at the graft-vein anastomosis of arteriovenous grafts (Lee and Roy-Chaudhury, Adv Chronic Kidney Dis 16(5):329–338, 2009). It is a physiological healing response to repeated vascular injury that results in increased stenosis. It is characterized by the activation, proliferation, and migration of cells from the medial layer to the intimal layer of the blood vessel wall. Roy-Chaudhury and colleagues have proposed that the pathophysiologic development of intimal hyperplasia in vascular access is due to a series of “upstream” and “downstream” events. There is also evidence to support a genetic role. This chapter will discuss these factors that are implicated in the development and progression of intimal hyperplasia.