Pharmacologic or cannulation strategies to prevent thrombosis of hemodialysis arteriovenous access
- Michael Allon, MD
Michael Allon, MD
- Professor of Medicine
- University of Alabama at Birmingham
- Section Editors
- Jeffrey S Berns, MD
Jeffrey S Berns, MD
- Editor-in-Chief — Nephrology
- Section Editor — Dialysis
- Professor of Medicine
- Perelman School of Medicine at the University of Pennsylvania
- David L Cull, MD
David L Cull, MD
- Section Editor — Arterial and Venous Access
- Clinical Professor, Department of Surgery
- University of South Carolina School of Medicine
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 AV grafts. (See "Overview of chronic hemodialysis vascular access".)
Hemodialysis AV access failure is primary due to irreversible thrombosis. More than 90 percent of thrombosed grafts have a stenotic lesion, suggesting that preemptive treatment of hemodynamically significant stenosis may prevent access thrombosis. However, this approach has been associated with disappointing results in randomized, controlled trials. (See "Endovascular intervention for the treatment of stenosis in the arteriovenous access" and "Techniques for angioplasty of the arteriovenous hemodialysis access".)
Alternative strategies to prevent graft thrombosis may be beneficial. This topic review provides an overview of pharmacologic or cannulation strategies to prevent vascular access thrombosis.
Vascular access stenosis of hemodialysis AV fistulas and grafts 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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