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Hemodialysis Vascular Access Dysfunction: Molecular Mechanisms and Treatment
Author(s) -
Mima Akira
Publication year - 2012
Publication title -
therapeutic apheresis and dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.415
H-Index - 53
eISSN - 1744-9987
pISSN - 1744-9979
DOI - 10.1111/j.1744-9987.2012.01066.x
Subject(s) - medicine , hemodialysis , neointimal hyperplasia , vascular access , arteriovenous fistula , anastomosis , endothelial dysfunction , stenosis , vein , fistula , intimal hyperplasia , pathogenesis , hemodialysis access , arteriovenous anastomosis , cardiology , surgery , intensive care medicine , stent , restenosis , smooth muscle
Hemodialysis vascular access complications are one of the main causes associated with an increase in morbidity and hospitalization in hemodialysis (HD) patients. The most common cause of vascular access dysfunction is venous stenosis as a result of venous neointimal hyperplasia within the peri‐anastomotic region (arteriovenous [AV] fistula) or at the graft‐vein anastomosis. There have been few studies regarding effective therapeutic interventions for HD vascular dysfunction at the present time, despite the magnitude of the clinical problem. This review will focus initially on the pathology and pathogenesis of HD vascular access dysfunction in the setting of both native AV fistula and polytetrafluoroethylene (PTFE) graft, then experimental and clinical therapies that could potentially be used in the setting of HD vascular access dysfunction.