Medical Innovation Center, TMK Project, Kyoto University, Kyoto, Japan; Department of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Department of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Semin Nephrol. 2020 Mar;40(2):206-215. doi: 10.1016/j.semnephrol.2020.01.011.
Acute kidney injury (AKI), defined as a rapid decrease in glomerular filtration rate, is a common and devastating pathologic condition. AKI is associated with significant morbidity and subsequent chronic kidney disease (CKD) development. Regardless of the initial insult, CKD progression after AKI involves multiple types of cells, including proximal tubular cells, fibroblasts, and immune cells. Although the mechanisms underlying this AKI to CKD progression have been investigated extensively over the past decade, therapeutic strategies still are lacking. One of the reasons for this stems from the fact that AKI and its progression toward CKD is multifactorial and variable because it is dependent on patient background. In this review, we describe the current understanding of AKI and its maladaptive repair with a focus on proximal tubules and resident fibroblasts. Subsequently, we discuss the unique pathophysiology of AKI in the elderly, highlighting our recent finding of age-dependent tertiary lymphoid tissues.
急性肾损伤（AKI），定义为肾小球滤过率的快速下降，是一种常见且具有破坏性的病理状况。AKI 与显著的发病率和随后的慢性肾脏病（CKD）的发展相关。无论初始损伤如何，AKI 后的 CKD 进展涉及多种类型的细胞，包括近端肾小管细胞、成纤维细胞和免疫细胞。尽管在过去十年中已经广泛研究了导致 AKI 向 CKD 进展的机制，但仍缺乏治疗策略。造成这种情况的原因之一是，AKI 及其向 CKD 的进展是多因素和可变的，因为它取决于患者的背景。在这篇综述中，我们描述了对 AKI 及其适应性修复的现有理解，重点是近端小管和固有成纤维细胞。随后，我们讨论了老年人 AKI 的独特病理生理学，强调了我们最近发现的与年龄相关的三级淋巴组织。
