Hemodialysis Vascular Access Dysfunction

A successful functioning vascular access is the “lifeline” for a hemodialysis patient. Hemodialysis vascular access dysfunction is a major cause of morbidity and mortality in hemodialysis patients1-3. Improving vascular access outcomes remains an ongoing challenge for nephrologists, vascular access surgeons, and interventionists. In arteriovenous fistulas (AVF) and grafts (AVG), the most common cause of this vascular access dysfunction is venous stenosis as a result of neointimal hyperplasia within the peri-anastomotic region (AVF) or at the graft-vein anastomosis (AVG) 4,5. There have been few effective treatments to-date for venous neointimal hyperplasia in part because of the poor understanding of the pathogenesis of venous neointimal hyperplasia. Central venous catheters (CVC) are prone to frequent thrombosis and infection and the treatment of catheter-related bacteremia (CRB) remains on ongoing debate 6-8. Therefore, this review will: (1) describe the pathology and pathophysiology of hemodialysis access stenosis in AVFs and AVGs, (2) discuss the pathogenesis of CRB and catheter thrombosis (3) discuss current and future novel therapies for treating venous neointimal hyperplasia, (4) discuss current strategies to treat CRB and catheter thrombosis, and (5) suggest future research areas in the field of hemodialysis vascular access dysfunction.