Preexisting Venous Calcification Prior to Dialysis Vascular Access Surgery
Department of Internal Medicine and Division of Nephrology and Hypertension, University of Cincinnati, Ohio Cincinnati Veterans Administration Medical Center, Cincinnati, Ohio Dialysis Vascular Access Research Group Cincinnati, Ohio Department of Surgery, University of Cincinnati, Ohio Department of Pathology, University of Cincinnati, Ohio.Seminars in Dialysis (Impact Factor: 1.75). 03/2012; 25(5):592-5. DOI: 10.1111/j.1525-139X.2012.01063.x
Vascular calcification is present in arterial vessels used for dialysis vascular access creation prior to surgical creation. Calcification in the veins used to create a new vascular access has not previously been documented. The objective of this study was to describe the prevalence of venous calcification in samples collected at the time of vascular access creation. Sixty-seven vein samples were studied. A von Kossa stain was performed to quantify calcification. A semi-quantitative scoring system from 0 to 4+ was used to quantify the percentage positive area for calcification as a fraction of total area (0: 0; 1+: 1-10%; 2+: 11-25%; 3+: 26-50%; 4+: >50% positive). Twenty-two of 67 (33%) samples showed evidence of venous calcification. Histologic examination showed varying degrees of calcification within each cell layer. Among the subset of patients with calcification, 4/22 (18%), 19/22 (86%), 22/22 (100%), and 7/22 (32%) had calcification present within the endothelium, intima, media, and adventitia, respectively. The mean semi-quantitative scores of the 22 samples with calcification were 0.18 ± 0.08, 1.2 ± 0.14, 1.6 ± 0.13, and 0.36 ± 0.12 for the endothelium, intima, media, and adventitia, respectively. Our results demonstrate that vascular calcification is present within veins used to create new dialysis vascular access, and located predominately within the neointimal and medial layers.
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ABSTRACT: The optimal vascular access for elderly patients remains a challenge due to the difficulty balancing the benefits and risks in a population with increased comorbidity and decreased survival. Age is commonly associated with failure to mature in fistula and decreased rates of primary and secondary patency in both fistula and grafts. In the elderly, at 1 and 2 years, primary patency rates range from 43% to 74% and from 29% to 67%, respectively. Secondary patency rates at 1 and 2 years range from 56% to 82% and 44% to 67%, respectively. Cumulative fistula survival is no better than grafts survival when primary failures are included. Several observational studies consistently demonstrate a lower adjusted mortality among those using a fistula compared with a catheter; however, catheter use in the elderly is increasing in most countries with the exception of Japan. Both guidelines and quality initiatives do not acknowledge the trade-offs involved in managing the elderly patients with multiple chronic conditions and limited life expectancy or the value that patients place on achieving these outcomes. The framework for choice of vascular access presented in this article considers: (1) likelihood of disease progression before death, (2) patient life expectancy, (3) risks and benefits by vascular access type, and (4) patient preference. Future studies evaluating the timing and type of vascular access with careful assessments of complications, functionality, cost benefit, and patients' preference will provide relevant information to individualize and optimize care to improve morbidity, mortality, and quality of life in the elderly patient.Seminars in Dialysis 11/2012; 25(6):640-648. DOI:10.1111/sdi.12037 · 1.75 Impact Factor
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ABSTRACT: Haemodialysis vascular access patency is severely compromised by fistula non-maturation and access stenosis. Intimal hyperplasia (IH) is considered the culprit lesion in failed fistulas, resulting in luminal narrowing and stenosis. This review focuses on the biology and pathophysiology of fistula failure and highlights not only the classically associated IH but also some relatively neglected but potentially important contributors such as inadequate outward remodelling. In addition, the complex process and fragile balance of successful fistula maturation might be partially hindered by pre-existent chronic kidney disease-mediated vasculopathy. Further unravelling the (patho)physiology of outward remodelling and IH could contribute to novel therapies and enhance fistula patency.Nephrology Dialysis Transplantation 03/2013; 28(5). DOI:10.1093/ndt/gft068 · 3.58 Impact Factor
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ABSTRACT: Background 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. Conclusions: In 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.Clinical Journal of the American Society of Nephrology 04/2013; 8(8). DOI:10.2215/CJN.11091012 · 4.61 Impact Factor
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