脓毒症相关急性肾损伤病理生理机制及生物标志物的研究进展

Research Progress on the Pathophysiological Mechanisms and Biomarkers of Acute Kidney Injury in Sepsis

摘要: 脓毒症相关急性肾损伤(SA-AKI)是一种急性功能障碍和器官损伤综合征，在ICU中，占所有AKI的一半。其发病机制仍然不太清楚，多种机制在不同患者及病程中以不同的强度作用，最终导致组织耐受，或者进一步导致肾小管、肾小球、足细胞损伤，从而产生不同的分型。脓毒症性AKI的主要诊断，包括尿量减少和血清肌酐水平升高。然而，这些指标可能受到多种因素的影响，血清肌酐对损伤的反应较慢，在功能损失超过50%之前不会发生变化，此外，肌肉质量、饮食、药物和脱水等因素影响。尿量无特异性，容易受到液体摄入量、药物和脱水等影响。这些缺点促使研究人员寻找新型AKI生物标志物，以及脓毒症相关生物标志物，以更早地检测脓毒症导致的肾脏应激或损伤，并预测SA-AKI的发展。

Abstract: Sepsis-associated acute kidney injury (SA-AKI) is a syndrome characterized by acute functional im-pairment and organ damage, accounting for half of all cases of acute kidney injury (AKI) in the ICU. The underlying mechanisms of SA-AKI are still not fully understood, as multiple mechanisms act with varying intensities in different patients and stages of the disease, ultimately leading to tissue tolerance or further injury to renal tubules, glomeruli, and podocytes, resulting in different sub-types. The primary diagnostic criteria for sepsis-related AKI include decreased urine output and elevated serum creatinine levels. However, these indicators may be influenced by various factors, and serum creatinine responds slowly to injury, not changing until functional loss exceeds 50%. Additionally, it is susceptible to factors such as muscle mass, diet, medications, and dehydration. Urine output lacks specificity and can be affected by factors such as fluid intake, medications, and dehydration. These limitations have prompted researchers to seek novel AKI biomarkers and sep-sis-related biomarkers to detect renal stress or injury caused by sepsis earlier and predict the de-velopment of SA-AKI.