Fistula failure in haemodialysis is driven not only by intimal hyperplasia but also by inadequate outward remodelling and pre-existent chronic kidney disease-mediated vasculopathy.
This review highlights that arteriovenous fistula failure is driven not only by intimal hyperplasia but also by inadequate outward remodeling and pre-existing CKD-mediated vasculopathy.
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.
Rothuizen et al. (Fri,) conducted a review in Haemodialysis vascular access failure. Fistula failure in haemodialysis is driven not only by intimal hyperplasia but also by inadequate outward remodelling and pre-existent chronic kidney disease-mediated vasculopathy.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: