Venous aneurysm complicating arteriovenous fistula access and matrix metalloproteinases

Abstract

IntroductionAn arteriovenous fistula (AVF) for placed for hemodialysis may be burdened by one particular complication—the formation of a venous aneurysm. It has been shown that matrix metalloproteinases (MMPs) and neutrophil gelatinase-associated lipocalin (NGAL) could represent markers of disease in both venous and arterial vessels.Materials and methodsThis case study reports a rare case of enormous venous aneurysm-correlated MMP and NGAL levels in a woman with an AVF.ResultsSignificantly higher levels of plasma MMP-1, MMP-8, MMP-9, and NGAL were detected in this patient during aneurysmal evaluation before the surgery; these levels significantly decreased 1, 3 and 6 months after surgery.ConclusionMMP and NGAL levels could represent a marker of aneurysmal disease, and their plasma evaluation could help physicians to stratify the risk of complications in patients with an AVF.

Expression of MMP-2, MMP-9, and NGAL in Tissue and Serum of Patients with Vascular Aneurysms and Their Modulation by Statin Treatment: A Pilot Study

“…An uncreated expression of MMPs causes loss of elastin and can induce compensatory fibrosis and inflammation with the destruction of all major matrix components, excessive distension, and vessel wall rupture [30][31][32]. In this view, recently, we documented that vascular damage induces an inflammatory response that can evoke a local reaction with the activation and recall of cytokines and inflammatory mediators [33] involved in aneurysmal diseases [32,34]. In an interesting pilot study, Yuwen et al [35], investigating the expression of a plethora of cytokines in patients with aortic aneurysmal disease compared to healthy patients, described the role of several cytokines (i.e., CC chemokines, CXC chemokines, proinflammatory cytokines, growth factors, proteolytic proteins, and cell adhesion cytokines) in the pathogenesis of the aneurysms.…”

Aneurysms in Vascular Access: State of the Art and Future Developments

“…The main driver of vessel remodeling is WSS, which increases rapidly following clamp release. Sustained increases in WSS results in the activation of enzymes via endothelial cell signaling, particularly matrix metalloproteases, which allow structural changes within the vein wall and result in dilatation and remodeling (2, 3). As the vessel diameter increases, the WSS decreases, which results in negative feedback.…”