Xu Xiaoqin, Zeng Tingting, Chen Si, Tian Na, Zhang Chunying, Chen Yuemei, Deng Shanying, Mao Zhigang, Liao Juan, Zhang Tonghao, He Yi, Wang Wei, Chen Pan, Song Yali
Department of Laboratory Medicine, Clinical Laboratory Medicine Research Center, West China Hospital, Sichuan University, Sichuan Clinical Research Center for Laboratory Medicine, Chengdu, Sichuan Province, 610041, People's Republic of China.
Department of Clinical Laboratory, Shanxi Province Cancer Hospital, Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences, Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, Shanxi Province, 030013, People's Republic of China.
Mol Biomed. 2025 Sep 5;6(1):61. doi: 10.1186/s43556-025-00293-4.
Acute kidney injury (AKI) is a prevalent clinical condition that is associated with unacceptably high morbidity and mortality, as well as the development of chronic kidney disease (CKD). The pathogenesis of AKI is highly complex and heterogeneous, primarily attributed to metabolic disturbances arising from the disease itself and the administration of medications related to treatment. In recent years, AKI in cancer patients is highly concerned. The emergence of AKI caused injuries and dysfunction of remote organs but also enhanced the health-care costs. It's essential for early recognition of AKI by biomarker or prediction models and further, take a timely intervention. This review aims to provide the pathophysiology of AKI covering the intricate mechanisms underpinning AKI in the dynamic context of the clinical setting, the tailored role of inflammation and ischemia, and the cellular and molecular crosstalk pathways involved. These events closely related to patients at high risk of AKI and underscore the characteristics that may make these patients more susceptible to injury. Furthermore, the diagnosis of AKI relies on clinical criteria, biomarkers, and imaging, but it should be distinguished from CKD. Finally, the review offers the therapeutic intervention in clinical practice and preclinical or clinical trials, focusing on the improvement of conventional therapy and advanced novel treatment strategies. Simultaneously, the challenge and future direction on early identifying renal impairment and performing renoprotection are also discussed, further supporting the novel discipline including onco-nephrology. The development of effective interventions that reduce nephrotoxicity is highly contingent upon a thorough understanding of the molecular pathophysiology of AKI.
急性肾损伤(AKI)是一种常见的临床病症,与高得令人难以接受的发病率和死亡率以及慢性肾脏病(CKD)的发生相关。AKI的发病机制高度复杂且具有异质性,主要归因于疾病本身引起的代谢紊乱以及与治疗相关的药物使用。近年来,癌症患者中的AKI备受关注。AKI的出现不仅导致远处器官的损伤和功能障碍,还增加了医疗成本。通过生物标志物或预测模型早期识别AKI并及时进行干预至关重要。本综述旨在阐述AKI的病理生理学,涵盖临床环境动态背景下AKI的复杂机制、炎症和缺血的特定作用以及所涉及的细胞和分子相互作用途径。这些事件与AKI高危患者密切相关,并突出了可能使这些患者更易受伤的特征。此外,AKI的诊断依赖于临床标准、生物标志物和影像学检查,但应与CKD相区分。最后,本综述介绍了临床实践以及临床前或临床试验中的治疗干预措施,重点是传统疗法的改进和先进的新型治疗策略。同时,还讨论了早期识别肾功能损害和实施肾脏保护方面的挑战及未来方向,进一步支持了包括肿瘤肾脏病学在内的新学科。开发有效的减少肾毒性的干预措施高度依赖于对AKI分子病理生理学的深入理解。