Highly increased cell proliferation activity in the restenotic hemodialysis vascular access after percutaneous transluminal angioplasty: implication in prevention of restenosis

Chang, Chi-Jen; Ko, Po‐Jen; Hsu, Lung‐An; Ko, Yu-Shien; Ko, Yu‐Lin; Chen, Chin-Fen; Huang, Chiu‐Ching; Hsu, Tsu‐Shiu; Lee, Ying-Shiung; Pang, Jong‐Hwei S.

doi:10.1053/j.ajkd.2003.09.015

Cited by 183 publications

(149 citation statements)

References 24 publications

Supporting

Mentioning

146

Contrasting

Order By: Relevance

“…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

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…Success rates are dismal (11,21,(52)(53)(54) because vessel injury to the endothelium and smooth muscle cells within the media that occurs after the PTA leads to further development of neointimal hyperplasia and restenosis (13,55). This suggests that although PTA may be important to treat stenosis in AVF and AVG, drug therapies may need to be applied to the site of angioplasty and endothelial injury to promote vascular healing and prolong vascular access patency.…”

Section: Endovascular Therapiesmentioning

confidence: 99%

“…Angioplasty is effective because its causes an aggressive outward remodeling (vasodilation) by rupturing the intima-media junction. Consequently, it also results in significant endothelial and medial smooth muscle cell damage, and the vessel wall invariably responds with an increased cellular proliferation within the neointima and, subsequently, a more aggressive neointimal hyperplasia development (13). Although most of the data on angioplasty-induced neointimal hyperplasia come from studying arterial models (14,15), it is also very likely that there is a deleterious injury from angioplasty to the venous system, especially because the venous tissue has intrinsically high baseline levels of inflammation and oxidative stress (16,17) from the uremic milieu.…”

Section: Histopathology Following Endovascular Repairmentioning

confidence: 99%

Novel Paradigms for Dialysis Vascular Access

Lee

2013

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

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.

show abstract

“…The stenotic vascular lesions that arise from this intimal hyperplastic response mainly consist of vascular smooth muscle cells, myofibroblasts, and extracellular matrix proteins (10). Excessive accumulation of extracellular matrix is mediated by several growth factors (5,9,11). Morphologically, these stenotic lesions closely resemble restenotic lesions after percutaneous coronary intervention (12,13).…”

Section: Introductionmentioning

confidence: 99%

Candidate Gene Analysis of Arteriovenous Fistula Failure in Hemodialysis Patients

Verschuren

Ocak²,

Dekker³

et al. 2013

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

SummaryBackground and objectives Arteriovenous fistula (AVF) failure remains an important cause of morbidity in hemodialysis patients. The exact underlying mechanisms responsible for AVF failure are unknown but processes like proliferation, inflammation, vascular remodeling, and thrombosis are thought to be involved. The current objective was to investigate the association between AVF failure and single nucleotide polymorphisms (SNPs) in genes related to these pathophysiologic processes in a large population of incident hemodialysis patients.Design, setting, participants, & measurements A total of 479 incident hemodialysis patients were included between January 1997 and April 2004. Follow-up lasted 2 years or until AVF failure, defined as surgery, percutaneous endovascular intervention, or abandonment of the vascular access. Forty-three SNPs in 26 genes, related to proliferation, inflammation, endothelial function, vascular remodeling, coagulation, and calcium/ phosphate metabolism, were genotyped. Relations were analyzed using Cox regression analysis.Results In total, 207 (43.2%) patients developed AVF failure. After adjustment, two SNPs were significantly associated with an increased risk of AVF failure. The hazard ratio (95% confidence interval) of LRP1 rs1466535 was 1.75 (1.15 to 2.66) and patients with factor V Leiden had a hazard ratio of 2.54 (1.41 to 4.56) to develop AVF failure. The other SNPs were not associated with AVF failure. ConclusionsIn this large cohort of hemodialysis patients, only 2 of the 43 candidate SNPs were associated with an increased risk of AVF failure. Whether other factors, like local hemodynamic circumstances, are more important or other SNPs play a role in AVF failure remains to be elucidated.

show abstract

Highly increased cell proliferation activity in the restenotic hemodialysis vascular access after percutaneous transluminal angioplasty: implication in prevention of restenosis

Cited by 183 publications

References 24 publications

The Effect of Lowering LDL Cholesterol on Vascular Access Patency

The Effect of Lowering LDL Cholesterol on Vascular Access Patency

Novel Paradigms for Dialysis Vascular Access

Candidate Gene Analysis of Arteriovenous Fistula Failure in Hemodialysis Patients

Contact Info

Product

Resources

About