• Users Online: 54
  • Print this page
  • Email this page
REVIEW ARTICLE
Year : 2019  |  Volume : 2  |  Issue : 2  |  Page : 33-41

Molecular targets for improving arteriovenous fistula maturation and patency


1 Department of Surgery and the Vascular Biology and Therapeutics Program, Yale School of Medicine, Yale University, New Haven, USA
2 Department of Surgery and the Vascular Biology and Therapeutics Program, Yale School of Medicine, Yale University, New Haven, USA; Department of Vascular Surgery, The Third Xiangya Hospital; Department of Vascular Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China
3 Department of Surgery and the Vascular Biology and Therapeutics Program, Yale School of Medicine, Yale University, New Haven, USA; Department of Vascular Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China
4 Department of Surgery and the Vascular Biology and Therapeutics Program, Yale School of Medicine, Yale University, New Haven, USA; Department of Vascular Ultrasonography, Xuanwu Hospital, Capital Medical University, Beijing, China
5 Department of Surgery and the Vascular Biology and Therapeutics Program, Yale School of Medicine, Yale University; Department of Surgery and of Cellular and Molecular Physiology, Yale School of Medicine, Yale University, New Haven; Department of Surgery, VA Connecticut Healthcare System, West Haven, USA

Correspondence Address:
Prof. Alan Dardik
Yale University School of Medicine, Department of Surgery and of Cellular and Molecular Physiology, 10 Amistad Street, Room 437, PO Box 208089, New Haven, CT 06520-8089
USA
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/VIT.VIT_9_19

Rights and Permissions

The increasing prevalence of chronic and end-stage renal disease creates an increased need for reliable vascular access; although arteriovenous fistulae (AVF) are the preferred mode of hemodialysis access, 60% fail to mature and only 50% remain patent at 1 year. Fistulae mature by diameter expansion and wall thickening; this outward remodeling of the venous wall in the fistula environment relies on a delicate balance of extracellular matrix remodeling, inflammation, growth factor secretion, and cell adhesion molecule upregulation in the venous wall. AVF failure occurs via two distinct mechanisms with early failure secondary to lack of outward remodeling, that is, insufficient diameter expansion or wall thickening, whereas late failure occurs with excessive wall thickening due to neointimal hyperplasia and insufficient diameter expansion in a previously functional fistula. In recent years, the molecular basis of AVF maturation and failure are becoming understood to develop potential therapeutic targets to aid maturation and prevent access loss. Erythropoietin-producing hepatocellular (Eph) carcinoma receptors, along with their ligands and ephrins, determine vascular identity and are critical for vascular remodeling in the embryo. Manipulation of Eph receptor signaling in adults, as well as downstream pathways, is a potential treatment strategy to improve the rates of AVF maturation and patency. This review examines our current understanding of molecular changes occurring following fistula creation, factors predictive of fistula success, and potential areas of intervention to decrease AVF failure.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed88    
    Printed3    
    Emailed0    
    PDF Downloaded19    
    Comments [Add]    

Recommend this journal