Background: Oxidative stress increases in patients with end-stage renal disease and exaggerates the related comorbidities.

Objective: The aim of the study was to evaluate the effects of supplementation with decaffeinated green tea extract (catechins) on hemodialysis-induced reactive oxygen species, atherosclerotic disease risk factors, and proinflammatory cytokines.

Design: We enrolled 6 healthy subjects and 54 hemodialysis patients for the study. First, the pharmacokinetics of one oral dose of catechins was compared between healthy subjects (n = 6) and hemodialysis patients (n = 10). Second, in the 10 hemodialysis patients, we compared the antioxidant effects of 3 different doses (0, 455, and 910 mg) of oral catechins with that of oral vitamin C (500 mg) during a hemodialysis session. Third, the other 44 hemodialysis patients participated in a 7-mo interventional study, in which 30 patients received placebo throughout and 14 patients received catechins (455 mg/d) from the third to the fifth month.

Results: After one oral dose, the hemodialysis patients (n = 10) had later peaks and slower decay of plasma catechins than did the healthy subjects. In the 10 hemodialysis patients, catechin supplementation reduced hemodialysis-enhanced plasma hypochlorous acid activity more effectively than did placebo or vitamin C. Between treatments with 455 or 910 mg catechins, no significant difference was found in the reduction of plasma hypochlorous acid activity. Catechins also significantly reduced proinflammatory cytokine expression enhanced by hemodialysis. In the 7-mo interventional study, the 14 patients who received daily supplementation of catechins for 3 mo had less predialysis plasma hydrogen peroxide activity, lower hypochlorous acid activity, and lower phosphatidylcholine hydroperoxide, C-reactive protein, and proinflammatory cytokine concentrations than did the 30 hemodialysis patients who received placebo.

Conclusion: Catechins reduce hemodialysis-induced production of hydrogen peroxide and hypochlorous acid, atherosclerotic disease risk factors, and proinflammation.