title: The molecular mechanisms of hemodialysis vascular access failure.
abstract: The arteriovenous fistula has been used for more than 50 years to provide vascular access for patients undergoing hemodialysis. More than 1.5 million patients worldwide have end stage renal disease and this population will continue to grow. The arteriovenous fistula is the preferred vascular access for patients, but its patency rate at 1 year is only 60%. The majority of arteriovenous fistulas fail because of intimal hyperplasia. In recent years, there have been many studies investigating the molecular mechanisms responsible for intimal hyperplasia and subsequent thrombosis. These studies have identified common pathways including inflammation, uremia, hypoxia, sheer stress, and increased thrombogenicity. These cellular mechanisms lead to increased proliferation, migration, and eventually stenosis. These pathways work synergistically through shared molecular messengers. In this review, we will examine the literature concerning the molecular basis of hemodialysis vascular access malfunction.
authors.affiliation: Vascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA.
authors.forename: Akshaar
authors.initials: A
authors.lastname: Brahmbhatt
authors.affiliation: Biomedical Engineering Department, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Bergamo, Italy.|Engineering Department, University of Bergamo, Dalmine, Italy.
authors.forename: Andrea
authors.initials: A
authors.lastname: Remuzzi
authors.affiliation: Biomedical Engineering Department, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Bergamo, Italy.
authors.forename: Marco
authors.initials: M
authors.lastname: Franzoni
authors.affiliation: Vascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA.|Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.|Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
authors.forename: Sanjay
authors.initials: S
authors.lastname: Misra
mesh_terms: D000818:Animals; D001166:Arteriovenous Shunt, Surgical / Q000009:adverse effects*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000628:therapy; D058426:Neointima / Q000209:etiology*; D006435:Renal Dialysis / Q000379:methods
keywords: arteriovenous fistula; murine model; restenosis; vascular biology; venous neointimal hyperplasia