Progress on the related mechanisms of vascular calcification in autogenous arteriovenous fistula in hemodialysis patients.

Autologous arteriovenous fistula (AVF) is the preferred vascular access for end-stage renal disease patients undergoing maintenance hemodialysis as a replacement therapy. As the duration of dialysis increases, the risk of vascular access-related complications such as AVF stenosis, thrombosis, vascular calcification (VC), and aneurysm formation gradually rises. Among these, VC has been proven to be independently associated with the occurrence and mortality of cardiovascular diseases in patients with chronic kidney disease (CKD). VC in the AVF of dialysis patients can lead to AVF failure, severely limiting its usability and increasing the risk of mortality among dialysis patients. Unlike previous reviews that predominantly focused on isolated mechanisms such as mineral metabolism or arterial calcification, this narrative review innovatively integrates the crosstalk among hemodynamic stress, inflammation, oxidative stress, deficiency of endogenous calcification inhibitors and pathological matrix remodeling, thereby providing a multidimensional perspective on AVF-VC. This review reframes the current understanding of AVF-VC, shifting it from a generalized complication of CKD-mineral and bone disorder to a distinct, fistula-specific pathological entity. This conceptual advancement offers a theoretical foundation for developing precision intervention strategies tailored to the unique microenvironment of the AVF.