Monocyte Chemoattractant Protein-1 Levels and Postangioplasty Restenosis of Arteriovenous Fistulas

Wu, Chih‐Cheng; Chen, Tsung Yan; Hsieh, Mu-Yang; Lin, Lin; Yang, Chung-Wei; Chuang, Shao Yuan; Tarng, Der Cheng

doi:10.2215/cjn.04030416

Cited by 13 publications

(14 citation statements)

References 42 publications

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“…104 The association of inflammatory markers and NIH has been demonstrated, but consistent literature in this setting is lacking. [105][106][107][108][109] An interesting recent paper from Hu et al 108 reported a positive correlation between IL-6 and AVF blood flow (Qa). In addition, besides a higher AVF Qa, higher inflammation levels were associated with cardiovascular morbidity.…”

Section: Inflammationmentioning

confidence: 98%

Factors affecting arteriovenous fistula dysfunction: A narrative review

Gameiro

Ibeas

2019

J Vasc Access

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Vascular access dysfunction is one of the most important causes of morbidity and mortality in haemodialysis patients, contributing to up to one third of hospitalisations and accounting for a significant amount of the health care costs of these patients. In the past decades, significant scientific advances in understanding mechanisms of arteriovenous fistula maturation and failure have contributed to an increase in the amount of research into techniques for creation and strategies for arteriovenous fistula dysfunction prevention and treatment, in order to improve patient care and outcomes. The aim of this review is to describe the pathogenesis of vascular access failure and provide a comprehensive analysis of the associated risk factors and causes of vascular access failure, in order to interpret possible future therapeutic approaches. Arteriovenous fistula failure is a multifactorial process resulting from the combination of upstream and downstream events with consequent venous neo-intimal hyperplasia and/or inadequate outward remodelling. Inflammation appears to be central in the biology of arteriovenous fistula dysfunction but important triggers still need to be revealed. Given the significant association of arteriovenous fistula failure and patient’s prognosis, it is therefore imperative to further research in this area in order to improve prevention, surveillance and treatment, and ultimately patient care and outcomes.

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Section: Inflammationmentioning

confidence: 98%

Factors affecting arteriovenous fistula dysfunction: A narrative review

Gameiro

Ibeas

2019

J Vasc Access

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“…The systemic changes of CKD, such as increased oxidative stress, changes in circulating cytokines, retention of toxic metabolites, and altered calcium homeostasis may be responsible for the structural and functional changes in the maturation of AV fistulas [14]. Previous studies have shown a negative impact of oxidative stress, cytokines, and calcium metabolism on neointima formation [15,16]. Nonetheless, the role of uremic toxins on venous intimal hyperplasia was less addressed.…”

Section: Discussionmentioning

confidence: 99%

Oral Charcoal Adsorbents Attenuate Neointima Formation of Arteriovenous Fistulas

Shih

Wang

et al. 2020

Toxins

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Chronic kidney disease (CKD) accelerates the development of neointima formation at the anastomosis site of arteriovenous (AV) fistulas. Accumulation of certain uremic toxins has a deleterious effect on the cardiovascular system. The oral charcoal adsorbent, AST-120, reduces circulating and tissue uremic toxins, but its effect on neointima formation at an AV fistula is unknown. To understand the effect of CKD and AST-120 on neointima formation, we created AV fistulas (common carotid artery to the external jugular vein in an end-to-side anastomosis) in mice with and without CKD. AST-120 was administered in chow before and after AV fistula creation. Administration of AST-120 significantly decreased serum indoxyl sulfate levels in CKD mice. CKD mice had a larger neointima area than non-CKD mice, and administration of AST-120 in CKD mice attenuated neointima formation. Both smooth muscle cell and fibrin components were increased in CKD mice, and AST-120 decreased both. RNA expression of MMP-2, MMP-9, TNFα, and TGFβ was increased in neointima tissue of CKD mice, and AST-120 administration neutralized the expression. Our results provided in vivo evidence to support the role of uremic toxin-binding therapy on the prevention of neointima formation. Peri-operative AST-120 administration deserves further investigation as a potential therapy to improve AV fistula patency.

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“…In hemodialysis patients, uraemia and dialysis are associated with increased oxidative stress that causes activation of inflammation, release of free radicals, and depletion of protective antioxidant. Recent studies have shown that pro-inflammatory chemokines and oxidative stress markers are implicated in venous intimal hyperplasia of dialysis vascular access 10,11,34 . Experimental studies also demonstrated that AA reduced oxidant stress levels, improved endothelial function, and decrease expression of vascular adhesion molecules, growth factors, and chemokines that may play an important role in the neointimal formation 35–37 .…”

Section: Discussionmentioning

confidence: 99%

“…Uraemia is associated with increased oxidative stress and depletion of protective antioxidants, which are further complicated by dialysis 9 . Recent studies have demonstrated that oxidative stress and inflammatory cytokines are implicated in the stenosis of dialysis access 10,11 . In animal studies, antioxidants have been shown to prevent restenosis after angioplasty 12–14 .…”

Section: Introductionmentioning

confidence: 99%

A randomized feasibility study of the effect of ascorbic acid on post-angioplasty restenosis of hemodialysis vascular access (NCT03524846)

Yang

Luo

et al. 2019

Sci Rep

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Restenosis remains a significant problem after angioplasty of hemodialysis vascular access. Both experimental and clinical studies have shown a protective effect of antioxidants against post-angioplasty restenosis. A prospective, randomized, feasibility study was conducted to investigate the effect of ascorbic acid to prevent restenosis. Ninety-three hemodialysis patients were randomized into three groups after angioplasty: placebo (n = 31), 300 mg ascorbic acid (n = 31), and 600 mg ascorbic acid (n = 31), treated intravenously 3 times per week for 3 months. Eighty-nine completed the clinical follow-up, and 81 had angiographic follow-up. In the angiographic follow-up, the mean (stand deviation) late loss of luminal diameter for the placebo, 300 mg, and 600 mg groups were 3.15 (1.68) mm, 2.52 (1.70) mm (P = 0.39 vs. placebo group), and 1.59 (1.67) mm (P = 0.006, vs. placebo group), with corresponding angiographic binary restenosis of 79%, 67% (P = 0.38 vs. placebo group), and 54% (P = 0.08 vs. placebo group). The post-interventional primary patency rates at 3 months were 47%, 55% (P = 0.59 vs. placebo group), and 70% (P = 0.18 vs. placebo group) for placebo, 300 mg, and 600 mg groups. Our results demonstrated that intravenous 600 mg ascorbic acid was a feasible therapy and might attenuate restenosis after angioplasty; however, its effect on post-interventional primary patency was modest.

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Monocyte Chemoattractant Protein-1 Levels and Postangioplasty Restenosis of Arteriovenous Fistulas

Abstract: Circulating monocyte chemoattractant protein-1 levels were elevated 2 days and 2 weeks after percutaneous transluminal angioplasty. Early postangioplasty increase of monocyte chemoattractant protein-1 level was associated with restenosis of arteriovenous fistulas.

Cited by 13 publications

References 42 publications

Factors affecting arteriovenous fistula dysfunction: A narrative review

Factors affecting arteriovenous fistula dysfunction: A narrative review

Oral Charcoal Adsorbents Attenuate Neointima Formation of Arteriovenous Fistulas

A randomized feasibility study of the effect of ascorbic acid on post-angioplasty restenosis of hemodialysis vascular access (NCT03524846)

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