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Thrombotic events and markers of oxidation and inflammation in hemodialysis
Author(s) -
Schwing William D,
Erhard Penny,
Holloman Cynthia K,
Weigel Kelly A,
Blankschaen Susan C,
Anderson James M,
Siegel Christopher T,
Seaman David S,
Valente John F,
DeOreo Peter B,
Weiss Miriam F
Publication year - 2004
Publication title -
hemodialysis international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.658
H-Index - 47
eISSN - 1542-4758
pISSN - 1492-7535
DOI - 10.1111/j.1492-7535.2004.80407.x
Subject(s) - medicine , pentosidine , hemodialysis , gastroenterology , vitamin e , vitamin d and neurology , vitamin , placebo , glycation , antioxidant , pathology , biochemistry , chemistry , receptor , alternative medicine
The goal of this study was to determine whether antioxidant therapy with vitamin E would alter the rate of vascular access complications or other macrovascular complications in hemodialysis (HD) patients. A secondary goal of the study was to explore the relationship between baseline pretreatment markers of oxidative stress (the advanced glycation end product pentosidine and basal levels of vitamin Eα and γ) and the subsequent development of access failure. Thirty‐five stable patients treated by HD were recruited for the study. Patients were provided with vitamin E (800 IU) or placebo capsules to be taken daily. Clinical variables, vascular access function (flow meter access flow measurements), and circulating blood markers were obtained initially and every 3 months throughout the study. Vitamin Eα levels rose in treated patients from 12.7 ± 4.4 to 25.1 ± 15.1 µg/mL at 3 months and 28.6 ± 14.8 µg/mL at 6 months. Vitamin Eγ levels fell in treated patients from 3.9 ± 1.7 to 2.3 ± 1.5 µg/mL at 3 months and 1.7 µg/mL at 6 months. Patients who subsequently developed repeated thrombotic vascular access events were characterized by higher baseline pentosidine content of circulating proteins. Patients who developed a myocardial infarction had higher pentosidine, lower vitamin Eα, and much lower vitamin Eγ than patients who did not develop thrombotic events. These findings lead to the speculation that the anti‐inflammatory effects of vitamin Eγ may play a more important role in thrombotic vascular events than the antioxidant effects of vitamin Eα. Additional studies of these interactions are in progress.