Hyperoxalemia Leads to Oxidative Stress in Endothelial Cells and Mice with Chronic Kidney Disease

<b><i>Introduction:</i></b> Cardiovascular disease is the most common cause of morbidity and mortality in patients with ESRD. In addition to phosphate overload, oxalate, a uremic toxin, also involved vascular calcification The present study investigated role mechanism hyperoxalemia mice uremia. <b><i>Methods:</i></b> A atherosclerosis (UA) model was established by left renal excision right electrocoagulation apoE<sup>−/−</sup> investigate relationship between oxalate loading calcification. After 12 weeks, serum levels calcification, inflammatory factors (TNF-α IL-6), oxidative stress markers (malondialdehyde [MDA], advanced oxidation protein products [AOPP]) were assessed UA mice. oral oxalate-degrading microbe <i>Oxalobacter formigenes</i> (<i>O. formigenes</i>) used evaluate effect reduction on underlying cultured human aortic endothelial cells (HAECs) smooth muscle (HASMCs). <b><i>Results:</i></b> Serum significantly increased Compared control mice, developed more areas showed significant increases factors. correlation analysis that positively correlated MDA, AOPP, TNF-α levels, negatively superoxide dismutase activity. <i>O. intervention decreased while did not improve significantly. addition, systemic inflammation improved group. vitro, high concentrations dose-dependently factor expression HAECs, but HASMCs. <b><i>Conclusions:</i></b> Our results indicated led activation stress. might be promising treatment for prevention deposition calcified