RENAL PROTECTIVE EFFECT AND CLINICAL ANALYSIS OF VITAMIN B6 IN PATIENTS WITH SEPSIS

医学 丙二醛 肌酐 败血症 血尿素氮 氧化应激 肾功能 胃肠病学 维生素C 内科学 维生素E 外科 抗氧化剂 生物化学 化学
作者
Yao Wang,Wen-Long Lu,Wenming Feng,Wei Xu,Lihua Liu,Li-Min He
出处
期刊:Shock [Lippincott Williams & Wilkins]
卷期号:61 (6): 841-847 被引量:3
标识
DOI:10.1097/shk.0000000000002329
摘要

ABSTRACT: Objective: To investigate the protective effect and possible mechanisms of vitamin B 6 against renal injury in patients with sepsis. Methods: A total of 128 patients with sepsis who met the entry criteria in multiple centers were randomly divided into experimental (intravenous vitamin B 6 therapy) and control (intravenous 0.9% sodium chloride therapy) groups based on usual care. Clinical data, the inflammatory response indicators interleukin 6 (IL-6), interleukin 8 (IL-8), tumor necrosis factor (TNF-α), and endothelin-1 (ET-1), the oxidative stress response indicators superoxide dismutase, glutathione and malondialdehyde, and renal function (assessed by blood urea nitrogen, serum creatinine, and renal resistance index monitored by ultrasound) were compared between the two groups. Results: After 7 d of treatment, the IL-6, IL-8, TNF-α, and ET-1 levels in the experimental group were significantly lower than those in the control group, the oxidative stress response indicators were significantly improved in the experimental group and the blood urea nitrogen, serum creatinine, and renal resistance index values in the experimental group were significantly lower than those in the control group ( P < 0.05). There was no statistical difference between the two groups in the rate of renal replacement therapy and 28 d mortality ( P > 0.05). However, the intensive care unit length of stay and the total hospitalization expenses in the experimental group were significantly lower than those in the control group ( P < 0.05). Conclusion: The administration of vitamin B 6 in the treatment of patients with sepsis attenuates renal injury, and the mechanism may be related to pyridoxine decreasing the levels of inflammatory mediators and their regulation by redox stress.
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