Department of Anesthesiology and Perioperative Medicine, PennState Health-Milton S. Hershey Medical Center, Hershey, PA, USA.
Department of Critical Care Medicine, Mayo Clinic, Phoenix, AZ, 85054, USA.
Pediatr Nephrol. 2018 Oct;33(10):1629-1639. doi: 10.1007/s00467-017-3774-5. Epub 2017 Aug 11.
Acute kidney injury (AKI) is a systemic disease occurring commonly in patients who are critically ill. Etiologies of AKI can be septic or aseptic (nephrotoxic, or ischemia-reperfusion injury). Recent evidence reveals that innate and adaptive immune responses are involved in mediating damage to renal tubular cells and in recovery from AKI. Dendritic cells, monocytes/macrophages, neutrophils, T lymphocytes, and B lymphocytes all contribute to kidney injury. Conversely, M2 macrophages and regulatory T cells are essential in suppressing inflammation, tissue remodeling and repair following kidney injury. AKI itself confers an increased risk for developing infection owing to increased production and decreased clearance of cytokines, in addition to dysfunction of immune cells themselves. Neutrophils are the predominant cell type rendered dysfunctional by AKI. In this review, we describe the bi-directional interplay between the immune system and AKI and summarize recent developments in this field of research.
急性肾损伤(AKI)是一种常见于重症患者的全身性疾病。AKI 的病因可以是感染性或非感染性的(肾毒性或缺血再灌注损伤)。最近的证据表明,固有和适应性免疫反应参与介导肾小管细胞损伤和 AKI 的恢复。树突状细胞、单核细胞/巨噬细胞、中性粒细胞、T 淋巴细胞和 B 淋巴细胞都有助于肾损伤。相反,M2 巨噬细胞和调节性 T 细胞在抑制肾损伤后的炎症、组织重塑和修复中是必不可少的。AKI 本身会增加感染的风险,这是由于细胞因子的产生增加和清除减少,以及免疫细胞自身功能障碍所致。中性粒细胞是 AKI 导致功能障碍的主要细胞类型。在这篇综述中,我们描述了免疫系统与 AKI 之间的双向相互作用,并总结了这一研究领域的最新进展。