Cellular phenotypes in human stenotic lesions from haemodialysis vascular access

Roy‐Chaudhury, Prabir; Wang, Yan; Krishnamoorthy, Mahesh; Zhang, Jianhua; Banerjee, Rupak K.; Munda, Rino; Heffelfinger, Sue C.; Arend, Lois J.

doi:10.1093/ndt/gfn708

Cited by 123 publications

(127 citation statements)

References 27 publications

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“…The average CHADS2 score was 1.6 1 for AF patients who developed VAT and 2.0 1.2 for AF patients without VAT events ( p 0.28). In addition, the CHADS2 score was not correlated to serum CRP levels in our study ( p 0.23, Pearson's correlation analysis), which can be explained by the different nature of thromboembolic events and VAT [26][27][28] . Neointimal hyperplasia may play a key role in the development of VAT, but not in thromboembolic events among AF patients.…”

Section: Discussioncontrasting

confidence: 66%

Atrial Fibrillation linked to Vascular access Thrombosis in Chronic Hemodialysis Patients

Chen

Liu

et al. 2011

JAT

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Section: Discussioncontrasting

confidence: 66%

Atrial Fibrillation linked to Vascular access Thrombosis in Chronic Hemodialysis Patients

Chen

Liu

et al. 2011

JAT

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“…Recurrent stenosis in AVGs is mostly attributed to the development of occlusive IH at the graft-vein anastomosis (15,54). As expected, the types of cells isolated from graft IH lesions include not only the typical myofibroblasts characteristic of AVF lesions and a small proportion of contractile VSMCs (,10%) but also, an abundance of macrophages (54).…”

Section: Preexisting Vascular Pathology and Avg Outcomesmentioning

confidence: 53%

“…These studies emphasized the profound histologic differences between preexisting and postoperative IH ( Figure 1). Postoperative lesions are recognized as eccentric concentrations of myofibroblasts in the intima of AVFs and AVGs (9,10,15), whereas the preexisting venous pathology consists of concentric accumulations of both myofibroblasts and contractile VSMCs underneath the endothelial line (10,13). The National Institute of Diabetes and Digestive and Kidney Diseases-funded multicenter, observational Hemodialysis Fistula Maturation (HFM) Study confirmed the high prevalence of preexisting IH in veins used to create an AVF in 370 patients with CKD.…”

Section: Ih Pathobiology Of Preexisting Ihmentioning

confidence: 90%

New Insights into Dialysis Vascular Access: Impact of Preexisting Arterial and Venous Pathology on AVF and AVG Outcomes

Vázquez-Padrón

Allon

2016

CJASN

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Despite significant improvements in preoperative patient evaluation and surgical planning, vascular access failure in patients on hemodialysis remains a frequent and often unforeseeable complication. Our inability to prevent this complication is, in part, because of an incomplete understanding of how preexisting venous and arterial conditions influence the function of newly created arteriovenous fistulas and grafts. This article reviews the relationship between three preexisting vascular pathologies associated with CKD (intimal hyperplasia, vascular calcification, and medial fibrosis) and hemodialysis access outcomes. The published literature indicates that the pathogenesis of vascular access failure is multifactorial and not determined by any of these pathologies individually. Keeping this observation in mind should help focus our research on the true causes responsible for vascular access failure and the much needed therapies to prevent it.

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“…1,[9][10][11] The formation of neointima results from endothelial activation, 23 inflammation, 17,19 increased cell proliferation and migration, and matrix accumulation. 35 The formation of excessive neointima plays a major role in the maturational failure of AVFs, in which the AVFs may never fully acquire the capacity to accommodate and sustain the heightened rate of blood flow required for effective dialysis; it also accounts for late AVF failure after variable periods of adequate function. 1,34 In the current studies we have expanded on our previous observations and demonstrated that ETS-1 expression is increased in a mouse model of AVF as well as in human AVFs.…”

Section: Discussionmentioning

confidence: 99%

The Transcription Factor E26 Transformation–Specific Sequence-1 Mediates Neointima Formation in Arteriovenous Fistula

Feng¹,

Chumley²,

Allon³

et al. 2014

Journal of the American Society of Nephrology

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Hemodialysis vascular access dysfunction contributes to increased morbidity and mortality in hemodialysis patients. Arteriovenous fistula (AVF) is the preferred type of vascular access for hemodialysis but has high rates of dysfunction, in part because of excessive neointima formation. The transcription factor E26 transformation-specific sequence-1 (ETS-1) is a mediator of proinflammatory responses in hypertension and endovascular injury. We examined the role of ETS-1 in the formation of neointima in AVF. Right carotid artery to internal jugular vein fistulas were created in C57BL/6 mice and assigned to treatment with an ETS-1-dominant negative peptide (ETS-DN), an inactive mutant peptide (ETS-MU), or vehicle (n=6 per group). After 7 and 21 days, AVFs or contralateral internal jugular veins were processed for PCR, immunofluorescence, immunohistochemistry, and morphometry. In AVFs, ETS-1 mRNA increased 2.5-fold at 7 days and 4-fold at 21 days. By immunofluorescence, we confirmed increased expression of ETS-1 predominantly in the neointima and overlying endothelium. Similarly, ETS-1 expression increased in human AVFs compared with normal veins. In mice, ETS-DN, but not ETS-MU, reduced neointima formation at days 7 and 21 and reduced the expression of nitric oxide synthase 2, NADPH oxidase (NOX) 2, NOX4, E-selectin, and monocyte chemotactic protein-1. Shear stress increased ETS-1 phosphorylation in human umbilical vein cells in a NOX-dependent manner, demonstrating a role for reactive oxygen species in ETS-1 activation. These results unveil the role of ETS-1 as a mediator of neointima formation in AVF and may result in the development of novel strategies for the treatment of AVF dysfunction.

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Cellular phenotypes in human stenotic lesions from haemodialysis vascular access

Cited by 123 publications

References 27 publications

Atrial Fibrillation linked to Vascular access Thrombosis in Chronic Hemodialysis Patients

Atrial Fibrillation linked to Vascular access Thrombosis in Chronic Hemodialysis Patients

New Insights into Dialysis Vascular Access: Impact of Preexisting Arterial and Venous Pathology on AVF and AVG Outcomes

The Transcription Factor E26 Transformation–Specific Sequence-1 Mediates Neointima Formation in Arteriovenous Fistula

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