Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; The Clinical Research, Investigation and Systems Modeling of Acute Illness Center, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; Excellence Center for Critical Care Nephrology, Division of Nephrology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand; Department of Laboratory Medicine, Chulalongkorn University, Bangkok, Thailand.
Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; The Clinical Research, Investigation and Systems Modeling of Acute Illness Center, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Kidney Int. 2019 Nov;96(5):1083-1099. doi: 10.1016/j.kint.2019.05.026. Epub 2019 Jun 7.
Sepsis-associated acute kidney injury (S-AKI) is a frequent complication of the critically ill patient and is associated with unacceptable morbidity and mortality. Prevention of S-AKI is difficult because by the time patients seek medical attention, most have already developed acute kidney injury. Thus, early recognition is crucial to provide supportive treatment and limit further insults. Current diagnostic criteria for acute kidney injury has limited early detection; however, novel biomarkers of kidney stress and damage have been recently validated for risk prediction and early diagnosis of acute kidney injury in the setting of sepsis. Recent evidence shows that microvascular dysfunction, inflammation, and metabolic reprogramming are 3 fundamental mechanisms that may play a role in the development of S-AKI. However, more mechanistic studies are needed to better understand the convoluted pathophysiology of S-AKI and to translate these findings into potential treatment strategies and add to the promising pharmacologic approaches being developed and tested in clinical trials.
脓毒症相关性急性肾损伤(S-AKI)是危重病患者的常见并发症,与不可接受的发病率和死亡率相关。S-AKI 的预防很困难,因为当患者寻求医疗救治时,大多数患者已经发生了急性肾损伤。因此,早期识别对于提供支持性治疗和限制进一步损伤至关重要。目前的急性肾损伤诊断标准的早期检测能力有限;然而,最近已经验证了新型肾脏应激和损伤生物标志物,可用于预测脓毒症患者的急性肾损伤风险和早期诊断。最近的证据表明,微血管功能障碍、炎症和代谢重编程是可能在 S-AKI 发展中起作用的 3 个基本机制。然而,需要更多的机制研究来更好地理解 S-AKI 复杂的病理生理学,并将这些发现转化为潜在的治疗策略,并增加正在临床试验中开发和测试的有前途的药物治疗方法。