The kidney has a remarkable ability of repair after acute kidney injury (AKI). However, when injury is severe or persistent, the repair is incomplete or maladaptive and may lead to chronic kidney disease (CKD). Maladaptive kidney repair involves multiple cell types and multifactorial processes, of which inflammation is a key component. In the process of inflammation, there is a bidirectional interplay between kidney parenchymal cells and the immune system. The extensive and complex crosstalk between renal tubular epithelial cells and interstitial cells, including immune cells, fibroblasts, and endothelial cells, governs the repair and recovery of the injured kidney. Further research in this field is imperative for the discovery of biomarkers and promising therapeutic targets for kidney repair. In this review, we summarize the latest progress in the immune response and inflammation during maladaptive kidney repair, analyzing the interaction between immune cells and intrinsic kidney cells, pointing out the potentialities of inflammation-related pathways as therapeutic targets, and discussing the challenges and future research prospects in this field.

急性肾损伤（AKI）后肾脏具有显着的修复能力。然而，当损伤严重或持续时，修复不完全或适应不良，并可能导致慢性肾脏病 (CKD)。适应不良的肾脏修复涉及多种细胞类型和多因素过程，其中炎症是关键组成部分。在炎症过程中，肾实质细胞与免疫系统之间存在双向相互作用。肾小管上皮细胞和间质细胞（包括免疫细胞、成纤维细胞和内皮细胞）之间广泛而复杂的串扰控制着受损肾脏的修复和恢复。该领域的进一步研究对于发现肾脏修复的生物标志物和有希望的治疗靶点至关重要。在这篇评论中，