Baseline plasma glycemic profiles but not inflammatory biomarkers predict symptomatic restenosis after angioplasty of arteriovenous fistulas in patients with hemodialysis

Wu, Chih‐Cheng; Wen, Szu-Chi; Yang, Chung-Wei; Pu, Shih-Yun; Tsai, Keh-Sung; Chen, Jaw-Wen

doi:10.1016/j.atherosclerosis.2009.10.021

Cited by 17 publications

(17 citation statements)

References 14 publications

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“…First, most of the cardiovascular risk factors were not correlated with the number of EPCs in our hemodialysis patients. Second, our data is consistent with previous studies demonstrating that cardiovascular risk factors do not predict venous intimal hyperplasia of hemodialysis vascular accesses [22]–[24].…”

Section: Discussionsupporting

confidence: 93%

The Impact of Endothelial Progenitor Cells on Restenosis after Percutaneous Angioplasty of Hemodialysis Vascular Access

Huang

Lai

et al. 2014

PLoS ONE

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ObjectiveWe prospectively investigate the relation between baseline circulating endothelial progenitor cells and the subsequent development of restenosis after angioplasty of hemodialysis vascular access.BackgroundEffect of angioplasty for hemodialysis vascular access is greatly attenuated by early and frequent restenosis. Circulating endothelial progenitor cells (EPCs) play a key role in vascular repair but are deficient in hemodialysis patients.MethodAfter excluding 14 patients due to arterial stenosis, central vein stenosis, and failed angioplasty, 130 patients undergoing angioplasty for dysfunctional vascular access were prospectively enrolled. Flow cytometry with quantification of EPC markers (defined as CD34+, CD34+KDR+, CD34+KDR+CD133+) in peripheral blood immediately before angioplasty procedures was used to assess circulating EPC numbers. Patients were followed clinically for up to one year after angioplasty.ResultsDuring the one-year follow-up, 95 patients (73%) received interventions for recurrent access dysfunction. Patients in the lower tertile of CD34+KDR+ cell count had the highest restenosis rates (46%) at three month (early restenosis), compared with patients in the medium and upper tertiles of CD34+KDR+ cell count (27% and 12% respectively, p = 0.002). Patients in the lower tertile of CD34+KDR+ cell count received more re-interventions during one year. Patients with early restenosis had impaired EPC adhesive function and increased senescence and apoptosis. In multivariate analysis, the CD34+KDR+ and CD34+KDR+CD133+ cell counts were independent predictors of target-lesion early restenosis.ConclusionOur results suggest that the deficiency of circulating EPCs is associated with early and frequent restenosis after angioplasty of hemodialysis vascular access.

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Section: Discussionsupporting

confidence: 93%

The Impact of Endothelial Progenitor Cells on Restenosis after Percutaneous Angioplasty of Hemodialysis Vascular Access

Huang

Lai

et al. 2014

PLoS ONE

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“…Baseline circulating inflammatory markers predict restenosis in patients with coronary artery diseases (13,28,29). Nonetheless, studies in dialysis AVFs reveal conflicting results (30)(31)(32)(33). A dissimilar pathogenic process of dialysis AVFs may account for the disparity in some way.…”

Section: Discussionmentioning

confidence: 99%

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

Chen²,

Hsieh

et al. 2016

CJASN

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“…A majority of patients on hemodialysis often have an underlying history of diabetes [9], and a recent study demonstrated that fistula patency was associated with optimal glycemic control [21]. Developing novel therapies to aid in reducing venous stenosis formation is important for improving patient outcomes.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia-Induced Modulation of the Physiognomy and Angiogenic Potential of Fibroblasts Mediated by Matrix Metalloproteinase-2: Implications for Venous Stenosis Formation Associated with Hemodialysis Vascular Access in Diabetic Milieu

et al. 2015

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Purpose: It is hypothesized that venous stenosis formation associated with hemodialysis vascular-access failure is caused by hypoxia-mediated fibroblast-to-myofibroblast differentiation accompanied by proliferation and migration, and that diabetic patients have worse clinical outcomes. The aim of this study was to determine the functional and gene expression outcomes of matrix metalloproteinase-2 (Mmp-2) silencing in fibroblasts cultured under hyperglycemia and euglycemia with hypoxic and normoxic stimuli. Materials and Methods: AKR-2B fibroblasts were stably transduced using lentivirus-mediated shRNA-Mmp-2 or scrambled controls and subjected to hypoxia or normoxia under hyperglycemic or euglycemic conditions for 24 and 72 h. Gene expression of vascular endothelial growth factor-A (Vegf-A), Vegfr-1, Mmp-2, Mmp-9 and tissue inhibitors of matrix metalloproteinases (Timps) were determined by RT-PCR. Collagen I and IV secretion and cellular proliferation and migration were determined. Results: Under hyperglycemic conditions, there is a significant reduction in the average gene expression of Vegf-A and Mmp-9, with an increase in Timp-1 at 24 h of hypoxia (p < 0.05) in Mmp-2-silenced fibroblasts when compared to controls. In addition, there is a decrease in collagen I and IV secretion and cellular migration. The euglycemic cells were able to reverse these findings. Conclusion: These findings demonstrate the rationale for using anti-Mmp-2 therapy in dialysis patients with hemodialysis vascular access in helping to reduce stenosis formation.

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Baseline plasma glycemic profiles but not inflammatory biomarkers predict symptomatic restenosis after angioplasty of arteriovenous fistulas in patients with hemodialysis

Cited by 17 publications

References 14 publications

The Impact of Endothelial Progenitor Cells on Restenosis after Percutaneous Angioplasty of Hemodialysis Vascular Access

The Impact of Endothelial Progenitor Cells on Restenosis after Percutaneous Angioplasty of Hemodialysis Vascular Access

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

Hyperglycemia-Induced Modulation of the Physiognomy and Angiogenic Potential of Fibroblasts Mediated by Matrix Metalloproteinase-2: Implications for Venous Stenosis Formation Associated with Hemodialysis Vascular Access in Diabetic Milieu

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