Sepsis-associated AKI is a life-threatening complication that is associated with high morbidity and mortality in patients who are critically ill. Although it is clear early supportive interventions in sepsis reduce mortality, it is less clear that they prevent or ameliorate sepsis-associated AKI. This is likely because specific mechanisms underlying AKI attributable to sepsis are not fully understood. Understanding these mechanisms will form the foundation for the development of strategies for early diagnosis and treatment of sepsis-associated AKI. Here, we summarize recent laboratory and clinical studies, focusing on critical factors in the pathophysiology of sepsis-associated AKI: microcirculatory dysfunction, inflammation, NOD-like receptor protein 3 inflammasome, microRNAs, extracellular vesicles, autophagy and efferocytosis, inflammatory reflex pathway, vitamin D, and metabolic reprogramming. Lastly, identifying these molecular targets and defining clinical subphenotypes will permit precision approaches in the prevention and treatment of sepsis-associated AKI.

脓毒症相关的 AKI 是一种危及生命的并发症，与危重患者的高发病率和死亡率相关。尽管败血症的早期支持性干预措施显然可以降低死亡率，但是否能预防或改善败血症相关的 AKI 尚不清楚。这可能是因为败血症引起的 AKI 的具体机制尚未完全了解。了解这些机制将为制定脓毒症相关 AKI 的早期诊断和治疗策略奠定基础。在这里，我们总结了最近的实验室和临床研究，重点关注脓毒症相关 AKI 病理生理学的关键因素：微循环功能障碍、炎症、NOD 样受体蛋白 3 炎性体、microRNA、细胞外囊泡、自噬和胞吞作用，炎症反射途径、维生素 D 和代谢重编程。最后，确定这些分子靶点并定义临床亚表型将有助于制定预防和治疗脓毒症相关 AKI 的精确方法。