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Asymmetric Dimethylarginine does not Predict Early Access Events in Hemodialysis Patients with Brachiocephalic Fistula Access.
Background: Vascular access for hemodialysis is best provided by an arteriovenous fistula (AVF). AVF fail primarily because of neointimal hyperplasia. Asymmetric dimethlyarginine (ADMA) is a naturally occurring analogue of L-arginine, which is elevated in renal failure and impairs endothelial cell function. ADMA inhibits nitric oxide synthetase, leading to impaired nitric oxide production and contributing to the development of neointimal hyperplasia. ADMA was measured at the time of AVF placement to evaluate associations with access failure.
Methods: ADMA was measured at the time of brachiocephalic access placement. Patients were followed for up to 12 months with end-points of access thrombosis or venous stenosis.
Results: Sixty patients with primary brachiocephalic fistulas were included in the study cohort. The median value for ADMA drawn at the time of AVF creation was 3.1 µmol/L. ADMA was not significantly associated with early thrombosis or venous stenosis events ( P >0.05).
Conclusion: Preoperative ADMA levels, as a surrogate for endothelial cell dysfunction and predictor of adverse access event (thrombosis or stenosis), were not associated with subsequent access events Future studies that identify markers of endothelial cell dysfunction are warranted.
Methods: ADMA was measured at the time of brachiocephalic access placement. Patients were followed for up to 12 months with end-points of access thrombosis or venous stenosis.
Results: Sixty patients with primary brachiocephalic fistulas were included in the study cohort. The median value for ADMA drawn at the time of AVF creation was 3.1 µmol/L. ADMA was not significantly associated with early thrombosis or venous stenosis events ( P >0.05).
Conclusion: Preoperative ADMA levels, as a surrogate for endothelial cell dysfunction and predictor of adverse access event (thrombosis or stenosis), were not associated with subsequent access events Future studies that identify markers of endothelial cell dysfunction are warranted.
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