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.

中文翻译：

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败血症引起的急性肾损伤：当前概念，流行病学，病理生理学，预防和治疗。

脓毒症相关的急性肾损伤（S-AKI）是重症患者的常见并发症，并与不可接受的发病率和死亡率相关。预防S-AKI十分困难，因为在患者寻求医疗救护时，大多数人已经发展为急性肾损伤。因此，早期识别对于提供支持治疗和限制进一步的伤害至关重要。当前急性肾损伤的诊断标准限制了早期发现。然而，最近已验证了肾脏压力和损害的新型生物标记物可用于败血症背景下的风险预测和急性肾损伤的早期诊断。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发生中起作用的3个基本机制。然而，