Hematopathology, Pathology Department, Center for Biomedical Diagnosis (CDB), Hospital Clinic, 08036 Barcelona, Spain.
Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, 08036, Spain.
Toxins (Basel). 2020 Jun 1;12(6):361. doi: 10.3390/toxins12060361.
Chronic kidney disease (CKD) patients have an accelerated atherosclerosis, increased risk of thrombotic-ischemic complications, and excessive mortality rates when compared with the general population. There is also evidence of an endothelial damage in which the proinflammatory state, the enhanced oxidative stress, or the accumulation of toxins due to their reduced renal clearance in uremia play a role. Further, there is evidence that uremic endothelial cells are both involved in and victims of the activation of the innate immunity. Uremic endothelial cells produce danger associated molecular patterns (DAMPS), which by binding to specific pattern recognition receptors expressed in multiple cells, including endothelial cells, induce the expression of adhesion molecules, the production of proinflammatory cytokines and an enhanced production of reactive oxygen species in endothelial cells, which constitute a link between immunity and inflammation. The connection between endothelial damage, inflammation and defective immunity in uremia will be reviewed here.
慢性肾脏病(CKD)患者的动脉粥样硬化加速,血栓形成-缺血性并发症风险增加,死亡率高于普通人群。此外,还有证据表明内皮细胞受损,其中促炎状态、增强的氧化应激,或由于尿毒症中肾脏清除减少而导致的毒素积累发挥了作用。此外,有证据表明尿毒症内皮细胞既是先天免疫激活的参与者,也是其受害者。尿毒症内皮细胞产生危险相关分子模式(DAMPS),通过与包括内皮细胞在内的多种细胞中表达的特定模式识别受体结合,诱导黏附分子的表达、促炎细胞因子的产生和内皮细胞中活性氧的产生增加,从而在免疫和炎症之间建立联系。本文将综述尿毒症中内皮损伤、炎症和免疫缺陷之间的联系。