Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMC

Cellular and molecular mechanisms underlying hemodialysis arteriovenous fistula dysfunction and approaches to promote maturation: a vascular perspective

Shiu YT., Northrup H., Huang Y., Cho ME., Bunsawat K.

Narrative Review on Chronic Kidney Disease, Chronic Inflammation, Autoimmune Research, published in Am J Physiol Heart Circ Physiol (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Am J Physiol Heart Circ Physiol (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40465509
PMCID
PMC12237592
DOI
10.1152/ajpheart.00010.2025
Citations
7

Abstract (original English)

Hemodialysis requires functional vascular access, which serves as the conduit for blood flow between the patient and the hemodialysis machine. The arteriovenous fistula (AVF), created by surgically connecting an artery to a nearby vein in the upper extremity, is the preferred form of vascular access for maintenance hemodialysis. Newly created AVFs must undergo a maturation process, during which the fistula vein enlarges and develops sufficient lumen size and blood flow to be used effectively for dialysis. However, since the invention of AVFs 60 years ago, rates of AVF maturation failure have remained high. Currently, no proven therapies exist to promote maturation or prevent maturation failure. This review examines the current understanding of the cellular and molecular mechanisms underlying AVF maturation failure, with particular focus on the impact of the chronic kidney disease (CKD) environment on the vascular system. In CKD, patients often have elevated levels of uremic toxins, increased oxidative stress, and chronic inflammation, all of which adversely affect the function of vascular wall cells (such as endothelial cells, vascular smooth muscle cells, and fibroblasts) and circulating cells (such as platelets and immune/inflammatory cells). The goal of this review is to explore the mechanisms influencing both native and AVF vasculature in the context of CKD. In addition, we

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AnimalsHumansRenal DialysisArteriovenous Shunt, SurgicalOxidative StressVascular PatencyRenal Insufficiency, Chronic

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