The molecular mechanisms of hemodialysis vascular access failure

Akshaar Brahmbhatt, Andrea Remuzzi, Marco Franzoni, Sanjay Misra

Research output: Contribution to journalReview articlepeer-review

83 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)303-316
Number of pages14
JournalKidney international
Issue number2
StatePublished - Feb 1 2016


  • arteriovenous fistula
  • murine model
  • restenosis
  • vascular biology
  • venous neointimal hyperplasia

ASJC Scopus subject areas

  • Nephrology


Dive into the research topics of 'The molecular mechanisms of hemodialysis vascular access failure'. Together they form a unique fingerprint.

Cite this