Tang Ying, Mak Shiu-Kwong, Xu An P, Lan Hui-Yao
Department of Nephrology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Shatin, Hong Kong.
Nephrology (Carlton). 2018 Oct;23 Suppl 4:50-52. doi: 10.1111/nep.13454.
Acute kidney injury (AKI) is characterized by both non-inflammatory and inflammatory process, and accumulating evidence has demonstrated that inflammation plays a key role in the pathogenesis and progression of AKI. C-reactive protein (CRP), an acute reactant produced by liver and many inflammatory cells, acts not only as an inflammation biomarker, but also as a pathogenic factor for AKI. Indeed, increased concentration of CRP is associated with poor outcome of varied etiologically related AKI patients. In recent years, the role of CRP is gradually recognized as an active participant in the pathogenesis and progression of AKI by exacerbating local inflammation, impairing the proliferation of damaged tubular epithelial cells and promoting fibrosis of injured renal tissue.
急性肾损伤（AKI）的特征在于非炎症和炎症过程，越来越多的证据表明炎症在AKI的发病机制和进展中起关键作用。C反应蛋白（CRP）是一种由肝脏和许多炎症细胞产生的急性反应物，不仅作为炎症生物标志物，还作为AKI的致病因素。事实上，CRP浓度升高与各种病因相关的AKI患者的不良预后有关。近年来，CRP的作用逐渐被认为是通过加剧局部炎症、损害受损肾小管上皮细胞的增殖以及促进受损肾组织的纤维化，从而积极参与AKI的发病机制和进展。
