4.7 Article

Oxidative stress, advanced glycation end product, and coronary artery calcification in hemodialysis patients

Journal

KIDNEY INTERNATIONAL
Volume 70, Issue 1, Pages 218-224

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1038/sj.ki.5000330

Keywords

oxidative stress; advanced glycation end product; coronary artery calcification; hemodialysis

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Coronary artery calcification is an index of the severity of atherosclerotic vascular disease, and may predict future adverse cardiovascular events in uremic patients undergoing hemodialysis (HD). HD patients are exposed to oxidative stress, and show high plasma levels of advanced glycation end products (AGEs). The association between oxidative stress, AGEs, established cardiovascular risk factors, and coronary artery calcification score (CACS) was studied in 225 HD patients (123 male, 102 female patients). CACS was measured by using multi-detector row computed tomography. Age, systolic blood pressure, calcium, calcium x phosphate, malondialdehyde, lipid peroxides, and pentosidine were significantly and positively correlated with CACS. Duration on HD tended to be positively correlated with CACS. From the independent variables included in the forward stepwise multiple linear regression analysis, only age, systolic blood pressure, lipid peroxides, calcium, and pentosidine were independently associated with CACS. The odds ratios for past history of coronary artery disease and the presence of diabetes mellitus for high CACS (>= 100) were 6.25 (95% confidence interval; 1.83-21.4) and 2.03 (95% confidence interval; 1.02-4.05), respectively. The plasma pentosidine was significantly and positively correlated with indoxyl sulfate. In conclusion, in addition to such traditional cardiovascular risk factors as past history, diabetes mellitus, aging, systolic blood pressure and calcium overload, oxidative stress ( lipid peroxides), and AGE ( pentosidine) are associated with extensive coronary artery calcification in HD patients. Lipid peroxidation and glycoxidation may be involved in the pathogenesis of coronary artery calcification.

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