El-Achkar T M, Hosein M, Dagher P C
Department of Medicine, Saint Louis University and Saint Louis VA Medical Centre, Missouri, USA.
Eur J Clin Invest. 2008 Oct;38 Suppl 2:39-44. doi: 10.1111/j.1365-2362.2008.02007.x.
Acute renal failure is a grave complication of systemic gram-negative sepsis. The pathophysiological mechanisms of sepsis leading to kidney injury result in part from systemic inflammatory and haemodynamic alterations. These are triggered by the interaction of endotoxin with Toll-like receptor 4 (TLR4) on cells of the immune system. Recently, TLR4 and other co-effector molecules were identified on renal tubular and vascular cells. Furthermore, it was demonstrated that systemic endotoxin has direct access to renal sites where these receptors are expressed. Therefore, we review data in support of this novel pathway of renal injury in sepsis, whereby systemic endotoxin causes direct injury through interactions with local epithelial and endothelial TLR4.
急性肾衰竭是全身性革兰氏阴性菌败血症的严重并发症。败血症导致肾损伤的病理生理机制部分源于全身性炎症和血流动力学改变。这些改变是由内毒素与免疫系统细胞上的Toll样受体4（TLR4）相互作用引发的。最近，在肾小管和血管细胞上发现了TLR4和其他协同效应分子。此外，已证明全身性内毒素可直接进入表达这些受体的肾脏部位。因此，我们综述了支持败血症中这种新的肾损伤途径的数据，即全身性内毒素通过与局部上皮和内皮TLR4相互作用导致直接损伤。
