The molecular mechanisms of hemodialysis vascular access failure

Akshaar Brahmbhatt, Andrea Remuzzi, Marco Franzoni, Sanjay Misra

Research output: Contribution to journalArticle

53 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)303-316
Number of pages14
JournalKidney International
Volume89
Issue number2
DOIs
StatePublished - Feb 1 2016

Fingerprint

Arteriovenous Fistula
Tunica Intima
Blood Vessels
Renal Dialysis
Hyperplasia
Uremia
Chronic Kidney Failure
Pathologic Constriction
Thrombosis
Inflammation
Population

Keywords

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

ASJC Scopus subject areas

  • Nephrology

Cite this

The molecular mechanisms of hemodialysis vascular access failure. / Brahmbhatt, Akshaar; Remuzzi, Andrea; Franzoni, Marco; Misra, Sanjay.

In: Kidney International, Vol. 89, No. 2, 01.02.2016, p. 303-316.

Research output: Contribution to journalArticle

Brahmbhatt, Akshaar ; Remuzzi, Andrea ; Franzoni, Marco ; Misra, Sanjay. / The molecular mechanisms of hemodialysis vascular access failure. In: Kidney International. 2016 ; Vol. 89, No. 2. pp. 303-316.
@article{b24ff87142b34fdc9afeb3aa39c3d387,
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.",
keywords = "arteriovenous fistula, murine model, restenosis, vascular biology, venous neointimal hyperplasia",
author = "Akshaar Brahmbhatt and Andrea Remuzzi and Marco Franzoni and Sanjay Misra",
year = "2016",
month = "2",
day = "1",
doi = "10.1016/j.kint.2015.12.019",
language = "English (US)",
volume = "89",
pages = "303--316",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Nature Publishing Group",
number = "2",

}

TY - JOUR

T1 - The molecular mechanisms of hemodialysis vascular access failure

AU - Brahmbhatt, Akshaar

AU - Remuzzi, Andrea

AU - Franzoni, Marco

AU - Misra, Sanjay

PY - 2016/2/1

Y1 - 2016/2/1

N2 - 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.

AB - 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.

KW - arteriovenous fistula

KW - murine model

KW - restenosis

KW - vascular biology

KW - venous neointimal hyperplasia

UR - http://www.scopus.com/inward/record.url?scp=84964661988&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84964661988&partnerID=8YFLogxK

U2 - 10.1016/j.kint.2015.12.019

DO - 10.1016/j.kint.2015.12.019

M3 - Article

C2 - 26806833

AN - SCOPUS:84964661988

VL - 89

SP - 303

EP - 316

JO - Kidney International

JF - Kidney International

SN - 0085-2538

IS - 2

ER -