Park Yohan, Zimmerman Kurt A, Miller Sarah J
Department of Internal Medicine, Division of Nephrology, University of Oklahoma Health Sciences Center, Oklahoma City, OK.
Department of Internal Medicine, Division of Nephrology, University of Oklahoma Health Sciences Center, Oklahoma City, OK.
Semin Nephrol. 2025 Sep 13:151666. doi: 10.1016/j.semnephrol.2025.151666.
Acute kidney injury (AKI) is a serious and common clinical condition characterized by a sudden decline in kidney function. Although kidney function decline is typically reversible, a certain subset of AKI patients eventually develop chronic kidney disease (CKD) and kidney failure. Immune cells are well-known mediators of injury sequelae. Myeloid cells such as neutrophils, dendritic cells, and macrophages drive the initial inflammatory response following AKI but can change their phenotype after resolution of the injury to promote repair. Failure to resolve the initial injury, or improper tubular repair, drives persistent myeloid cell accumulation that can result in the development of kidney fibrosis and CKD. In this review, we focus on the role of myeloid cells following AKI including the mechanisms through which they promote injury and repair.
急性肾损伤（AKI）是一种严重且常见的临床病症，其特征为肾功能突然下降。尽管肾功能下降通常是可逆的，但一定比例的AKI患者最终会发展为慢性肾脏病（CKD）和肾衰竭。免疫细胞是损伤后遗症的众所周知的介质。中性粒细胞、树突状细胞和巨噬细胞等髓系细胞在AKI后引发初始炎症反应，但在损伤消退后可改变其表型以促进修复。未能解决初始损伤或肾小管修复不当会导致髓系细胞持续积聚，进而可能导致肾纤维化和CKD的发展。在本综述中，我们重点关注AKI后髓系细胞的作用，包括它们促进损伤和修复的机制。
