BACKGROUND: Cardiovascular disease, and mainly coronary heart disease (CHD), is the leading cause of death in hemodialysis (HD) patients. Non-traditional risk factors may play an important role in this population. Arginase is known to contribute directly to atherosclerosis progression and to counteract the beneficial effects of nitric oxide. HD could be considered as an inflammatory condition. Inflammation contributes to atherosclerosis progression and influences both arginase and nitric oxide synthase expression. In the present study, serum arginase type I was evaluated as a marker of CHD in HD patients. The markers of inflammation interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were also assessed. PATIENTS AND METHODS: Sixty-eight HD patients and 24 healthy volunteers were enrolled into the study. Twenty HD patients suffered from CHD confirmed with coronary angiography, while the remaining 48 HD patients were asymptomatic. Serum arginase type I, IL-6 and TNF-α were measured with ELISA. During 24 months follow-up, none of the asymptomatic subjects developed symptoms of CHD. RESULTS: IL-6 and TNF-α levels were increased in HD patients, but did not differ between HD patients with or without CHD. On the contrary, arginase levels did not differ between healthy subjects and HD patients, but were twice higher in HD patients with CHD than in HD patients without CHD (22.41 ± 15.47 ng/ml vs. 10.16 ± 8.13 ng/ml). CONCLUSION: Arginase type I may contribute to the pathogenesis of CHD in HD patients and its serum levels could be used as a marker of CHD in this population.
BACKGROUND:Cardiovascular disease, and mainly coronary heart disease (CHD), is the leading cause of death in hemodialysis (HD) patients. Non-traditional risk factors may play an important role in this population. Arginase is known to contribute directly to atherosclerosis progression and to counteract the beneficial effects of nitric oxide. HD could be considered as an inflammatory condition. Inflammation contributes to atherosclerosis progression and influences both arginase and nitric oxide synthase expression. In the present study, serum arginase type I was evaluated as a marker of CHD in HDpatients. The markers of inflammationinterleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were also assessed. PATIENTS AND METHODS: Sixty-eight HDpatients and 24 healthy volunteers were enrolled into the study. Twenty HDpatients suffered from CHD confirmed with coronary angiography, while the remaining 48 HDpatients were asymptomatic. Serum arginase type I, IL-6 and TNF-α were measured with ELISA. During 24 months follow-up, none of the asymptomatic subjects developed symptoms of CHD. RESULTS:IL-6 and TNF-α levels were increased in HDpatients, but did not differ between HDpatients with or without CHD. On the contrary, arginase levels did not differ between healthy subjects and HDpatients, but were twice higher in HDpatients with CHD than in HDpatients without CHD (22.41 ± 15.47 ng/ml vs. 10.16 ± 8.13 ng/ml). CONCLUSION: Arginase type I may contribute to the pathogenesis of CHD in HDpatients and its serum levels could be used as a marker of CHD in this population.
Authors: C Zoccali; S Bode-Böger; F Mallamaci; F Benedetto; G Tripepi; L Malatino; A Cataliotti; I Bellanuova; I Fermo; J Frölich; R Böger Journal: Lancet Date: 2001 Dec 22-29 Impact factor: 79.321
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