Uremic Toxin Binder Breaks the Dead Linkage between Chronic Kidney Disease and Cardiovascular Disease by Ameliorating Monocyte Activation

摘要

Accumulated evidences demonstrated that oxi-dative stress is one of the most potent factors leading to endothelial dysfunction and is involved in all stages of atherosclerotic plaque evolution (1). Oxidative stress is caused by an imbalance between oxidant production, including reactive oxygen species (ROS) and antioxidant defense mechanism. Chronic kidney disease (CKD) patients are associated with an increased generation of oxidants, which led to chronic inflammation (2, 3). Monocyte chronic inflammation has been shown to play an important role in the development of cardiovascular disease (4). CKD patients are found to have increased proinflammatory T cells and monocytes. These cells might cause inflammation and destabilization of atherosclerotic plaques, and have been identified as novel non-classical cardiovascular risk factors in CKD subjects (5). A recent study in Taiwan showed that about 45% of dialysis patients died of cardiovascular disease (6). Decreasing monocyte chronic inflammation is a critical issue for improving the survival of CKD patients.