Division of Nephrology, Johns Hopkins Hospital, Johns Hopkins University School of Medicine, Ross 965, 720 Rutland Ave, Baltimore, MD, 21206, USA.
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
J Nephrol. 2020 Dec;33(6):1171-1187. doi: 10.1007/s40620-020-00793-2. Epub 2020 Jul 10.
Acute kidney injury (AKI) is an increasing health burden with high morbidity and mortality rates worldwide. AKI is a risk factor for chronic kidney disease (CKD) development and progression to end stage renal disease (ESRD). Rapid action is required to find treatment options for AKI, plus to anticipate the development of CKD and other complications. Therefore, it is essential to understand the pathophysiology of AKI to CKD transition. Over the last several years, research has revealed maladaptive repair to be an interplay of cell death, endothelial dysfunction, tubular epithelial cell senescence, inflammatory processes and more-terminating in fibrosis. Various pathological mechanisms have been discovered and reveal targets for potential interventions. Furthermore, there have been clinical efforts measures for AKI prevention and progression including the development of novel biomarkers and prediction models. In this review, we provide an overview of pathophysiological mechanisms involved in kidney fibrosis. Furthermore, we discuss research gaps and promising therapeutic approaches for AKI to CKD progression.
急性肾损伤 (AKI) 是全球范围内发病率和死亡率都很高的日益严重的健康负担。AKI 是慢性肾脏病 (CKD) 发展和进展为终末期肾病 (ESRD) 的危险因素。需要迅速采取行动，为 AKI 寻找治疗选择，并预测 CKD 和其他并发症的发展。因此，了解 AKI 向 CKD 转变的病理生理学至关重要。在过去的几年中，研究表明，适应性修复是细胞死亡、内皮功能障碍、肾小管上皮细胞衰老、炎症过程等的相互作用-最终导致纤维化。已经发现了各种病理机制，并揭示了潜在干预的靶点。此外，已经有针对 AKI 预防和进展的临床措施，包括新型生物标志物和预测模型的开发。在这篇综述中，我们提供了涉及肾脏纤维化的病理生理学机制的概述。此外，我们讨论了 AKI 向 CKD 进展的研究空白和有前途的治疗方法。
