الفهرس 
Chronic Kidney DiseaseOnly 14 pages are availabe for public view
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Abstract
Failure of hemodialysis (HD) vascular access (VA) is the dominant cause of morbidity and the major cost of care for ESRD patients (1). Surgical thrombectomy remains the standard treatment for salvage of the thrombosed AVF. However, the mid- or long-term patency rate after thrombectomy is unsatisfactory (2). In the Canadian HD Morbidity Study, hypoalbuminemia was the strongest predictor of arteriovenous graft (AVG) thrombosis (3). It is now well accepted that hypoalbuminemia is not only an indicator of malnutrition in uremic patients but also occurs as a result of inflammation (4). These observations indirectly support that inflammation might play some role in the thrombosis of AVF (5). Over the past four decades, significant progress has been made in the understanding of VA biology and techniques for creating and maintaining VA, but effective treatments to prevent VA failure are currently still lacking (6). The majority of AVF fail because of intimal hyperplasia. (7) In recent years, there have been many studies investigating the molecular mechanisms responsible for intimal hyperplasia and subsequent thrombosis. These studies have identified common pathways including inflammation, uremia, hypoxia, sheer stress, and increased thrombogenicity. These pathways work synergistically through shared molecular messengers (8) .