Common pathological background of chronic kidney disease and life-habit associated metabolic disorders

慢性肾脏疾病（CKD）和与生活方式相关的代谢紊乱（如高血压和糖尿病）是心血管事件过多的独立危险因素，但其共同的病理机制或致病分子仍有待研究。本研究鉴定了葡萄糖降解分子？甲基乙二醛是候选之一。甲基乙二醛通过增强氧化应激诱导细胞和器官损伤。此外，甲基乙二醛的降解过程可能促进嘌呤代谢，导致尿酸的产生。

Chronic kidney disease (CKD) and life-style related metabolic disorders such as hypertension, and diabetes, are independent risk factors for excess cardiovascular events, however the common pathological mechanisms or causative molecules have remained to be addressed. The present study identified glucose degraded molecule ? methylglyoxal as one of the candidates. Methylglyoxal induces cellular and organ damage by enhancing oxidative stress. Furthermore, it was suggested that the degraded process of methylglyoxal may facilitate purine metabolism, leading to uric acid production.