New Insights into Dialysis Vascular Access: Molecular Targets in Arteriovenous Fistula and Arteriovenous Graft Failure and Their Potential to Improve Vascular Access Outcomes

Lee, Timmy; Misra, Sanjay

doi:10.2215/cjn.02030216

Cited by 55 publications

(54 citation statements)

References 80 publications

(97 reference statements)

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“…This study showed that the cumulative VA patency after VAIVT was significantly higher in patients treated with antiplatelet agents than in those who were not treated with antiplatelet agents. This outcome is biologically plausible because several recent reports have suggested that high levels of local oxidative stress or inflammatory mediators are involved in development of VAF [35][36][37][38][39]. Several recent studies showed that some mediators such as heme oxygenase-1 and heme oxygenase-2, monocyte chemoattractant protein-1, Kruppel-like factor-2, and TGF-b1 play an important role in AVF dysfunction in mouse model [40,41].…”

Section: Discussionmentioning

confidence: 85%

Patency with antiplatelet treatment after vascular access intervention therapy: a retrospective observational study

et al. 2018

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Background: Vascular access (VA) intervention therapy (VAIVT) has been increasingly used for treating VA failure (VAF) in patients undergoing hemodialysis; however, clinical evidence demonstrating the efficacy of prevention of VAF after VAIVT is limited. Therefore, we aimed to assess characteristics of patients developing VAF after VAIVT and analyze risk factors for VAF after VAIVT. Methods: This retrospective study included 96 patients with VAF who underwent ultrasound-guided VAIVT by interventional nephrologists between January 2013

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Section: Discussionmentioning

confidence: 85%

Patency with antiplatelet treatment after vascular access intervention therapy: a retrospective observational study

et al. 2018

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“…In particular, the process of OR plays a pivotal role in this process. Although past research has focused mainly on the development of strategies to reduce IH, the current view on AVF maturation underscores the link between impaired OR and AVF failure (42,43). To promote OR, matrix metalloproteinase expression must be augmented to degrade and restructure the vascular matrix (44), which is largely composed of elastic fibers.…”

Section: Impaired Elastin Degradation and Vascular Remodeling In Rxfpmentioning

confidence: 99%

Relaxin receptor deficiency promotes vascular inflammation and impairs outward remodeling in arteriovenous fistulas

et al. 2018

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The pathophysiology of arteriovenous fistula (AVF) maturation failure is not completely understood but impaired outward remodeling (OR) and intimal hyperplasia are thought to be contributors. This adverse vascular response after AVF surgery results from interplay between vascular smooth muscle cells (VSMCs), the extracellular matrix (ECM), and inflammatory cells. Relaxin (RLN) is a hormone that acts on the vasculature via interaction with RLN/insulin-like peptide family receptor 1 (RXFP1), resulting in vasodilatation, ECM remodeling, and decreased inflammation. In the present study, we evaluated the consequences of RXFP1 knockout ( Rxfp1) on AVF maturation in a murine model of AVF failure. Rxfp1 mice showed a 22% decrease in vessel size at the venous outflow tract 14 d after AVF surgery. Furthermore, a 43% increase in elastin content was observed in the lesions of Rxfp1 mice and coincided with a 41% reduction in elastase activity. In addition, Rxfp1 mice displayed a 6-fold increase in CD45 leukocytes, along with a 2-fold increase in monocyte chemoattractant protein 1 (MCP1) levels, when compared with wild-type mice. In vitro, VSMCs from Rxfp1 mice exhibited a synthetic phenotype, as illustrated by augmentation of collagen, fibronectin, TGF-β, and platelet-derived growth factor mRNA. In addition, VSMCs derived from Rxfp1 mice showed a 5-fold increase in cell migration. Finally, RXFP1 and RLN expression levels were increased in human AVFs when compared with unoperated cephalic veins. In conclusion, RXFP1 deficiency hampers elastin degradation and results in induced vascular inflammation after AVF surgery. These processes impair OR in murine AVF, suggesting that the RLN axis could be a potential therapeutic target for promoting AVF maturation.-Bezhaeva, T., de Vries, M. R., Geelhoed, W. J., van der Veer, E. P., Versteeg, S., van Alem, C. M. A., Voorzaat, B. M., Eijkelkamp, N., van der Bogt, K. E., Agoulnik, A. I., van Zonneveld, A.-J., Quax, P. H. A., Rotmans, J. I. Relaxin receptor deficiency promotes vascular inflammation and impairs outward remodeling in arteriovenous fistulas.

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“…Nevertheless, obtaining a functioning vascular access is not always easy. In fact, the failure of autogenous Vascular Access (aVA) maturation depends on many, and mostly unknown, factors [2]. Prosthetic Vascular Access (pVA) could represent a valuable alternative to aVA in case of maturation failure, thrombosis or poor vascular network [3].…”

Section: Introductionmentioning

confidence: 99%

Prosthetic Vascular Access Creation: Learning Curve Analysis

Franchin¹,

Tozzi²,

Mozzetta³

et al. 2019

Angiol Open Access

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Aim: In the present study, we analysed the learning curve of prosthetic vascular access creation. Materials and methods: The first 50 consecutive prosthetic vascular access created by a single experienced vascular surgeon was included in this study. Primary outcomes were operative time, intervention-free access survival and functional access survival. Additional outcomes were complications of the intervention. We used the cumulative sum technique to assess the learning curve. Results: The analysis of the learning curve obtained with cumulative sum technique on operative time, interventionfree survival and functional access survival permitted to define three phases: learning (first 25 patients), expertise (following 15 patients) and post-learning phase. Accordingly, statistical differences were observed in operative time, intervention-free survival, and frequencies of graft thrombosis among the three groups. Conclusion: Prosthetic vascular access creation is a safe and effective intervention when performed by an experienced vascular surgeon. Otherwise, a twenty-five interventions learning curve is mandatory to obtain better results in terms of operative time, circuit survival and frequency of thrombosis. Additional fifteen interventions are required to obtain an expert level of practice, allowing for more challenging procedure.

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New Insights into Dialysis Vascular Access: Molecular Targets in Arteriovenous Fistula and Arteriovenous Graft Failure and Their Potential to Improve Vascular Access Outcomes

Cited by 55 publications

References 80 publications

Patency with antiplatelet treatment after vascular access intervention therapy: a retrospective observational study

Patency with antiplatelet treatment after vascular access intervention therapy: a retrospective observational study

Relaxin receptor deficiency promotes vascular inflammation and impairs outward remodeling in arteriovenous fistulas

Prosthetic Vascular Access Creation: Learning Curve Analysis

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