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Molecular Mechanisms of Hemodialysis Graft Failure

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Abstract

Today there are more than 400,000 patients with end-stage renal disease (ESRD) in the United States, and the vast majority of patients use long-term hemodialysis as their mode of renal replacement therapy [1]. This population is expected to double in the next decade. For patients using chronic hemodialysis as their mode of renal replacement therapy, a highly functioning vascular access is their “lifeline” because it ensures adequate reduction of uremic toxins and maintenance of appropriate electrolyte balances. Hemodialysis vascular access dysfunction occurs in patients and is frequently caused by the development of venous stenosis at the vein-to-graft anastomosis site or in the proximal outflow vein [2].

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Acknowledgment

The project described was supported by Award Number R01HL098967 (SM) from the National Heart, Lung, And Blood Institute and a CR20 grant which is funded by 1UL1RR024150 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and the NIH Roadmap for Medical Research. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, And Blood Institute or the National Institutes of Health.

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Correspondence to Sanjay Misra MD, FSIR .

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Misra, S. (2011). Molecular Mechanisms of Hemodialysis Graft Failure. In: Rajan, D. (eds) Essentials of Percutaneous Dialysis Interventions. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-5657-6_6

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