Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, London, UK; MRC London Institute of Medical Sciences, Imperial College London, London, UK.
Centre for Nephrology, University College London, London, UK.
Kidney Int. 2017 Oct;92(4):809-815. doi: 10.1016/j.kint.2017.03.053. Epub 2017 Aug 12.
Patients with chronic kidney disease (CKD) have an enhanced risk of cardiovascular (CV) morbidity and mortality when compared with age- and gender-matched individuals with normal kidney function. Trimethlyamine N-oxide (TMAO) is a gut-derived amine oxide that has been implicated in the causation of CV diseases. Plasma TMAO is cleared by the kidney, and TMAO levels are elevated in CKD. Experimental studies have identified pathogenic mechanisms by which TMAO may contribute to CV disease through dysregulation of lipid metabolism, enhanced macrophage foam cell formation, and platelet dysfunction. Safe and well-tolerated therapeutic interventions such as pre- and probiotics, which modify the gut microbiome, offer the opportunity for interventional studies. This review examines the pathogenicity of TMAO, its value as a biomarker, and its potential as a therapeutic target in the context of CKD.
与肾功能正常的年龄和性别匹配的个体相比，慢性肾脏病（CKD）患者的心血管（CV）发病率和死亡率更高。三甲胺 N-氧化物（TMAO）是一种肠道衍生的胺氧化物，与 CV 疾病的发生有关。血浆 TMAO 由肾脏清除，CKD 患者的 TMAO 水平升高。实验研究已经确定了 TMAO 通过脂质代谢失调、增强巨噬细胞泡沫细胞形成和血小板功能障碍导致 CV 疾病的致病机制。益生菌和益生元等安全且耐受良好的治疗干预措施可以改变肠道微生物组，为干预研究提供机会。本综述探讨了 TMAO 的致病性、作为生物标志物的价值以及在 CKD 背景下作为治疗靶点的潜力。
