Strategies other than treatment of stenosis to prevent thrombosis of hemodialysis vascular access grafts
- Michael Allon, MD
Michael Allon, MD
- Professor of Medicine
- University of Alabama at Birmingham
Hemodialysis requires access to blood vessels capable of providing rapid extracorporeal blood flow. These requirements are currently best met by both primary arteriovenous (AV) fistulas and synthetic grafts. (See "Overview of chronic hemodialysis vascular access".)
Access failure is primary due to irreversible thrombosis. More than 90 percent of thrombosed grafts have a stenotic lesion, which is commonly treated with percutaneous transluminal angioplasty and/or surgery. However, mechanical approaches that rely upon preemptive angioplasty to treat stenosis to help graft failure are associated with disappointing results. Thus, alternative strategies to prevent graft thrombosis may be beneficial.
Strategies to prevent thrombosis of hemodialysis AV grafts other than treatment of the stenosis are presented in this topic review. Management of stenosis of hemodialysis access is presented separately.
Vascular access stenosis of a hemodialysis arteriovenous (AV) graft is initiated by endothelial cell injury, which leads to the upregulation of adhesion molecules on the endothelial cell surface. Subsequent leukocyte adherence to damaged and activated endothelium causes the release of chemotactic and mitogenic factors for vascular smooth muscle cells, thereby enhancing smooth muscle cell migration and proliferation [1-3].
Additional factors that contribute to the neointimal proliferation and fibromuscular hyperplasia include shear stress generated by the turbulent blood flow [4,5] and the mismatch in elastic properties around the anastomosis leading to excessive mechanical stretch . Activated platelets and inflammatory cells also secrete oxidants and other toxins that directly injure the vessel wall . Finally, angioplasty of stenotic lesions exacerbates neointimal hyperplasia, resulting in accelerated restenosis .
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