The Biology of Hemodialysis Vascular Access Failure

Arteriovenous fistulas (AVFs) are essential for patients and clinicians faced with end-stage renal disease (ESRD). While this method of vascular access for hemodialysis is preferred to others due to its reduced rate of infection and complications, they are plagued by intimal hyperplasia. The pathogenesis of intimal hyperplasia and subsequent thrombosis is brought on by uremia, hypoxia, and shear stress. These forces upregulate inflammatory and proliferative cytokines acting on leukocytes, fibroblasts, smooth muscle cells, and platelets. This activation begins initially with the progression of uremia, which induces platelet dysfunction and primes the body for an inflammatory response. The vasculature subsequently undergoes changes in oxygenation and shear stress during AVF creation. This propagates a strong inflammatory response in the vessel leading to cellular proliferation. This combined response is then further subjected to the stressors of cannulation and dialysis, eventually leading to stenosis and thrombosis. This review aims to help interventional radiologists understand the biological changes and pathogenesis of access failure.