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Arteriovenous access failure: more than just intimal hyperplasia?
Tonia C Rothuizen1, Chunyu Wong, Paul H A Quax
1Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Insights
Fistula failure in haemodialysis is often due to intimal hyperplasia (IH) and poor outward remodelling. Understanding these processes could lead to new therapies for better fistula patency.
Area of Science:
- Vascular Biology
- Nephrology
- Surgical Access
Background:
- Haemodialysis vascular access patency is critical for patient survival.
- Fistula non-maturation and access stenosis are major complications.
- Intimal hyperplasia (IH) is a primary cause of fistula failure.
Purpose of the Study:
- To review the biology and pathophysiology of fistula failure.
- To highlight intimal hyperplasia (IH) and inadequate outward remodelling.
- To explore the impact of chronic kidney disease-mediated vasculopathy.
Main Methods:
- Literature review of fistula maturation and failure.
- Analysis of biological mechanisms contributing to stenosis.
- Examination of vascular remodelling processes.
Main Results:
- Intimal hyperplasia (IH) causes luminal narrowing and stenosis.
- Inadequate outward remodelling is a significant, often overlooked, factor.
- Chronic kidney disease-associated vasculopathy may impair fistula maturation.
Conclusions:
- Understanding outward remodelling and IH is key to improving fistula patency.
- Novel therapies targeting these mechanisms could enhance haemodialysis access.
- Further research into fistula failure pathophysiology is warranted.
Abstract:
Haemodialysis vascular access patency is severely compromised by fistula non-maturation and access stenosis. Intimal hyperplasia (IH) is considered the culprit lesion in failed fistulas, resulting in luminal narrowing and stenosis. This review focuses on the biology and pathophysiology of fistula failure and highlights not only the classically associated IH but also some relatively neglected but potentially important contributors such as inadequate outward remodelling. In addition, the complex process and fragile balance of successful fistula maturation might be partially hindered by pre-existent chronic kidney disease-mediated vasculopathy. Further unravelling the (patho)physiology of outward remodelling and IH could contribute to novel therapies and enhance fistula patency.
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