Effect of Omega-3 Fatty Acids on Kidney Function after Myocardial Infarction: The Alpha Omega Trial
Effect of Omega-3 Fatty Acids on Kidney Function after Myocardial Infarction: The Alpha Omega Trial
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DOI：
10.2215/cjn.10441013
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发表时间：
2014-10-01
影响因子：
9.8
通讯作者：
Giltay, Erik J.
中科院分区：
文献类型：
--
作者：
Hoogeveen, Ellen K.;Geleijnse, Johanna M.;Giltay, Erik J.
背景和目的 肾功能随着年龄的增长而逐渐下降，心肌梗塞加速了这种恶化。 Omega-3 (n-3) 脂肪酸可以减缓肾功能的衰退。研究了海洋和植物源性 n-3 脂肪酸对心肌梗塞后患者肾功能的影响。 设计、设置、参与者和测量 在 Alpha Omega 试验中，2344 名年龄在 60-80 岁之间有心肌梗塞病史的患者（81% 为男性）被随机分配到四种试验人造黄油中的一种。患者接受额外目标量的 400 mg/d 二十碳五烯酸和二十二碳六烯酸、2 g/d α-亚麻酸、二十碳五烯酸-二十二碳六烯酸加 a-亚麻酸或安慰剂，为期 40 个月。在基线和 40 个月后评估血清胱抑素 C 和血清肌酐。使用慢性肾脏病流行病学协作方程估算基于肌酐-胱抑素 C 的 GFR。 结果 在积极治疗组中，患者每天消耗 19.9 g 人造黄油，额外提供 239 mg/d 二十碳五烯酸和 159 mg/d 二十二碳六烯酸、1.99 g/d α-亚麻酸，或两者均提供。 40 个月后，与基线相比，安慰剂、二十碳五烯酸-二十二碳六烯酸中基于肌酐-胱抑素 C 的平均 GFR 为 -6.9 (+/- 12.6)、-4.8 (+/- 13.4)、-6.2 (+/- 12.8) 和 -6.0 (+/- 13.0) ml/min 每 1.73 m(2)。分别是α-亚麻酸和二十碳五烯酸-二十二碳六烯酸加α-亚麻酸基团。 40 个月后，与安慰剂相比，接受二十碳五烯酸-二十二碳六烯酸治疗的患者中，基于肌酐-胱抑素 C 的 GFR 降低了 2.1（95% 置信区间，0.6 至 3.6；P
Background and objectives Kidney function gradually decreases with age, and myocardial infarction accelerates this deterioration. Omega-3 (n-3) fatty acids may slow down the decline of kidney function. The effect of marine and plant-derived n-3 fatty acids on kidney function in patients after myocardial infarction was examined.Design, setting, participants, & measurements In the Alpha Omega Trial, 2344 patients with history of myocardial infarction ages 60-80 years old (81% men) were randomized to one of four trial margarines. The patients received an additional targeted amount of 400 mg/d eicosapentaenoic acid and docosahexaenoic acid, 2 g/d a-linolenic acid, eicosapentaenoic acid-docosahexaenoic acid plus a-linolenic acid, or placebo for 40 months. Serum cystatin C and serum creatinine were assessed at baseline and after 40 months. Creatinine-cystatin C-based GFR was estimated with the Chronic Kidney Disease Epidemiology Collaboration equation.Results Patients consumed 19.9 g margarine/d, providing an additional 239 mg/d eicosapentaenoic acid with 159 mg/d docosahexaenoic acid, 1.99 g/d alpha-linolenic acid, or both in the active treatment groups. After 40 months, compared with baseline, mean (+/- SD) creatinine-cystatin C-based GFR was -6.9 (+/- 12.6), -4.8 (+/- 13.4), -6.2 (+/- 12.8), and -6.0 (+/- 13.0) ml/min per 1.73 m(2) in the placebo, eicosapentaenoic acid-docosahexaenoic acid, a-linolenic acid, and eicosapentaenoic acid-docosahexaenoic acid plus a-linolenic acid groups, respectively. After 40 months, in patients receiving eicosapentaenoic acid-docosahexaenoic acid compared with placebo, the decline in creatinine-cystatin C-based GFR was 2.1 less (95% confidence interval, 0.6 to 3.6; P