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      Oral Adsorbent AST-120 Decreases Carotid Intima-Media Thickness and Arterial Stiffness in Patients with Chronic Renal Failure

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          Background/Aim: Intima media thickness (IMT) and stiffness of the carotid arteries is related to coronary artery disease, and chronic renal failure patients are at high risk for such diseases. An oral adsorbent, AST-120 (Kremezin; Kureha Chemical Industry, Tokyo, Japan), can delay the progression of chronic renal failure in undialyzed uremic patients. The aim of the present study was to determine whether AST-120 affects carotid artery IMT and pulse wave velocity (PWV) in patients with chronic renal failure not undergoing dialysis. Methods: Fifty patients with non-diabetic chronic renal failure were randomly divided into two groups: 30 patients (18 men and 12 women; mean age 53.5 years; mean serum creatinine 3.2 mg/dl) who were given AST-120 (6.0 g/day) and 20 patients (12 men and 8 women; mean age 52.0 years; mean serum creatinine 3.5 mg/dl) who were not given AST-120. Thirty healthy age-matched subjects (18 men and 12 women; mean age 51.5 years; mean serum creatinine 0.9 mg/dl) were also included. The treatment period was 24 months. IMT and arterial stiffness were measured before and after treatment. Results: The slope of the reciprocal serum creatinine concentration over time became significantly less steep in the AST-120 group than in the non-AST-120 group (p < 0.001). Before treatment, carotid artery IMT differed little between the AST-120 group (0.90 ± 0.22 mm) and the non-AST-120 group (0.88 ± 0.20 mm). IMT in these two groups was significantly greater than IMT in the control group (0.64 ± 0.14 mm) (p < 0.01). Carotid IMT in the AST-120 group decreased slightly but not significantly to 0.84 ± 0.20 mm after 12 months and then significantly after 24 months to 0.78 ± 0.18 mm (p < 0.05). Carotid IMT in the non-AST group showed little change throughout the experimental period. PWV differed little between the AST-120 group (1,980 ± 330 cm/s) and the non-AST group (1,940 ± 360 cm/s) before treatment. PWV values in these two groups were significantly greater than PWV in the control group (1,280 ± 240 cm/s) (p < 0.01). After 12 and 24 months, PWV in the AST-120 group decreased significantly to 1,840 ± 280 cm/s (p < 0.05) and to 1,780 ± 260 cm/s (p < 0.05), respectively; however, PWV in the non-AST group showed a slight increase during the experimental period. Conclusion: The data suggest that AST-120 may reduce arterial stiffness and IMT in non-diabetic chronic renal failure patients before dialysis.

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          Most cited references 13

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          Influences of age and gender on results of noninvasive brachial-ankle pulse wave velocity measurement--a survey of 12517 subjects.

          The present study was conducted to evaluate the influences of age and gender on the results of noninvasive brachial-ankle pulse wave velocity (baPWV). In 12517 subjects who had no medication and no history of cardiovascular diseases, multiple regression analysis demonstrated that age, blood pressure, body mass index, triglycerides, blood glucose, and uric acid were significant variables for baPWV in both genders. From this population, we extracted 7881 "healthy subjects" (4488 males and 3393 females, 25-87 years) without any of the atherogenic risk factors, and the results of baPWV were analyzed chronologically in 5-year age intervals. baPWV was lower in females than in males until age 60, and became similar in both genders over age 60. Multiple regression analysis demonstrated that not only the value of R(2) but also the coefficient of the effect of age on baPWV are larger in females than in males. In the estimation of the regression curve, the relationship between age and baPWV demonstrated a quadratic curve in both genders. Thus, aging influences baPWV, and its effect is more prominent in female. Menopause seems to be the crucial phenomenon to explain the augmented increase in arterial stiffness with aging in females.
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            Clinical value of aortic pulse-wave velocity measurement.

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              Advanced atherosclerosis in predialysis patients with chronic renal failure.

              Atherosclerosis is advanced in hemodialysis patients as shown by increased intima-media thickness of carotid arteries (CA-IMT), although it is not established whether the advanced atherosclerosis results from hemodialysis treatment or from chronic renal failure. The purpose of this study was to evaluate the effects of hemodialysis and renal failure on CA-IMT in patients with chronic renal failure. CA-IMT was measured by high-resolution B-mode ultrasonography in 110 patients with chronic renal failure before starting dialysis (CRF group), and compared with CA-IMT of 345 hemodialysis patients (HD group) and 302 healthy control subjects. They were all nondiabetic and the three groups were comparable in age and gender. As compared with the healthy control subjects, the CRF and HD groups had greater CA-IMTs, whereas CA-IMTs of the CRF and HD groups were not statistically different. There was no significant correlation between duration of hemodialysis and CA-IMT in the HD group. Multiple regression analysis in the total subjects indicated that presence of renal failure, but not being treated with hemodialysis, was a significant factor associated with increased CA-IMT independent of age, gender, blood pressure, smoking, high-density lipoprotein (HDL) and non-HDL cholesterol levels. These results demonstrate that thickening of arterial wall is present in patients with chronic renal failure before starting hemodialysis treatment, and support the concept that advanced atherosclerosis in hemodialysis patients is due not to hemodialysis treatment, but to renal failure and/or metabolic abnormalities secondary to renal failure.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                July 2004
                03 May 2004
                : 27
                : 2
                : 121-126
                aDepartment of Medicine, Shinmatsudo Central General Hospital, Chiba; bDepartment of Pathology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, and cDepartment of Medicine, Koto Hospital, Tokyo, Japan
                77536 Kidney Blood Press Res 2004;27:121–126
                © 2004 S. Karger AG, Basel

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                Figures: 1, Tables: 4, References: 27, Pages: 6
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