Venous neointimal hyperplasia in polytetrafluoroethylene dialysis grafts

Roy‐Chaudhury, Prabir; Kelly, Burnett S.; Miller, Mary Ann; Reaves, Anita; Armstrong, Janice; Nanayakkara, N.; Heffelfinger, Sue C.

doi:10.1046/j.1523-1755.2001.00750.x

Cited by 326 publications

(291 citation statements)

References 26 publications

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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: 67%

“…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). Very few studies have evaluated the effect of preexisting vascular pathologies on AVG functional outcomes (Table 1).…”

Section: Preexisting Vascular Pathology and Avg Outcomesmentioning

confidence: 74%

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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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Section: Preexisting Vascular Pathology and Avg Outcomesmentioning

confidence: 67%

Section: Preexisting Vascular Pathology and Avg Outcomesmentioning

confidence: 74%

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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“…Neointimal hyperplasia, the main reason for loss of patency of both AVF and AV grafts, is induced by a cascade of inflammatory mediators that are the consequence of injury from surgery, increased hemodynamic stress, and/or repeated needling. The venous stenoses that result are characterized by the proliferation of smooth muscle cells with a myofibroblastic phenotype, as well as their migration (with macrophages) into the vessel's intima (16)(17)(18). Statin-based therapy might slow progression of neointimal hyperplasia by reducing vascular smooth muscle cell proliferation (19)(20)(21)(22)(23), smooth muscle cell migration (22), and monocyte activation (24), effects that are not known to be mediated through the LDL-C-lowering effect of hepatic hydroxymethyl glutaryl-CoA reductase inhibition.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Lowering LDL Cholesterol on Vascular Access Patency

Herrington¹,

Emberson²,

Staplin³

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives Reducing LDL cholesterol (LDL-C) with statin-based therapy reduces the risk of major atherosclerotic events among patients with CKD, including dialysis patients, but the effect of lowering LDL-C on vascular access patency is unclear.Design, setting, participants, & measurements The Study of Heart and Renal Protection (SHARP) randomized patients with CKD to 20 mg simvastatin plus 10 mg ezetimibe daily versus matching placebo. This study aimed to explore the effects of treatment on vascular access occlusive events, defined as any access revision procedure, access thrombosis, removal of an old dialysis access, or formation of new permanent dialysis access.Results Among 2353 SHARP participants who had functioning vascular access at randomization, allocation to simvastatin plus ezetimibe resulted in a 13% proportional reduction in vascular access occlusive events ( Conclusions Exploratory analyses from SHARP suggest that lowering LDL-C with statin-based therapy may improve vascular access patency, but there was no evidence of benefit in AURORA. Taken together, the available evidence suggests that any benefits of lowering LDL-C on vascular access patency are likely to be modest.

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“…Venous stenosis in AVGs most commonly arises from progressive neointimal hyperplasia, characterized by the presence of myofibroblasts and an abundance of extracellular matrix components within the neointima ( Figure 2C). Angiogenesis (neovascularization) within the adventitia and macrophage layer lining the perigraft region is also present in AVGs, which is the major difference from venous stenosis in AVFs (12).…”

Section: Avgsmentioning

confidence: 99%

Novel Paradigms for Dialysis Vascular Access

Lee

2013

Clinical Journal of the American Society of Nephrology

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SummaryVascular access dysfunction is a major cause of morbidity and mortality in hemodialysis patients. The most common cause of vascular access dysfunction is venous stenosis from neointimal hyperplasia within the perianastomotic region of an arteriovenous fistula and at the graft-vein anastomosis of an arteriovenous graft. There have been few, if any, effective treatments for vascular access dysfunction because of the limited understanding of the pathophysiology of venous neointimal hyperplasia formation. This review will (1) describe the histopathologic features of hemodialysis access stenosis; (2) discuss novel concepts in the pathogenesis of neointimal hyperplasia development, focusing on downstream vascular biology; (3) highlight future novel therapies for treating downstream biology; and (4) discuss future research areas to improve our understanding of downstream biology and neointimal hyperplasia development.

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Venous neointimal hyperplasia in polytetrafluoroethylene dialysis grafts

Cited by 326 publications

References 26 publications

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

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

The Effect of Lowering LDL Cholesterol on Vascular Access Patency

Novel Paradigms for Dialysis Vascular Access

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