Mary Hammes, Rita McGill, Promila Dhar, Rama S Madhurapantula
{"title":"不对称二甲基精氨酸不能预测血液透析患者头臂瘘通路的早期通路事件。","authors":"Mary Hammes, Rita McGill, Promila Dhar, Rama S Madhurapantula","doi":"10.16966/2380-5498.141","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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 (<i>P</i>>0.05).</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":92052,"journal":{"name":"International journal of nephrology and kidney failure","volume":"3 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5667913/pdf/","citationCount":"0","resultStr":"{\"title\":\"Asymmetric Dimethylarginine does not Predict Early Access Events in Hemodialysis Patients with Brachiocephalic Fistula Access.\",\"authors\":\"Mary Hammes, Rita McGill, Promila Dhar, Rama S Madhurapantula\",\"doi\":\"10.16966/2380-5498.141\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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 (<i>P</i>>0.05).</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":92052,\"journal\":{\"name\":\"International journal of nephrology and kidney failure\",\"volume\":\"3 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5667913/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International journal of nephrology and kidney failure\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.16966/2380-5498.141\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2017/4/6 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of nephrology and kidney failure","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.16966/2380-5498.141","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2017/4/6 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
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.