联合肾细胞阻滞和损伤生物标志物预测脓毒症患者进行性 AKI。
Combining renal cell arrest and damage biomarkers to predict progressive AKI in patient with sepsis.
机构信息
Division of Nephrology, Nanfang Hospital, Southern Medical University, National Clinical Research Center for Kidney Disease, State Key Laboratory of Organ Failure Research, Guangdong Provincial Clinical Research Center for Kidney Disease, Guangzhou Regenerative Medicine and Health-Guangdong Laboratory, 1838 North Guangzhou Ave, Guangzhou, 510515, China.
Department of Intensive Care Unit of Cardiovascular Surgery, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Laboratory of South China Structural Heart Disease, Department of Critical Care Medicine, Guangdong Provincial People's Hospital, Academy of Medical Sciences, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, 510000, Guangdong, China.
出版信息
BMC Nephrol. 2021 Dec 15;22(1):415. doi: 10.1186/s12882-021-02611-8.
BACKGROUND
Sepsis is the most common trigger for AKI and up to 40% of mild or moderate septic AKI would progress to more severe AKI, which is associated with significantly increased risk for death and later CKD/ESRD. Early identifying high risk patients for AKI progression is a major challenge in patients with septic AKI.
METHODS
This is a prospective, multicenter cohort study which enrolled adult patients with sepsis and initially developed stage 1 or 2 AKI in the intensive care unit from January 2014 to March 2018. AKI was diagnosed and staged according to 2012 KDIGO-AKI guidelines. Renal cell arrest biomarkers (urinary TIMP2IGFBP7, u[TIMP-2][IGFBP7]) and renal damage biomarkers (urinary KIM-1[uKIM-1] and urinary IL-18 [uIL-18]) were measured at time of AKI clinical diagnosis, and the performance of biomarkers for predicting septic AKI progression alone or in combination were evaluated. The primary outcome was AKI progression defined as worsening of AKI stage. The secondary outcome was AKI progression with subsequent death during hospitalization.
RESULTS
Among 433 screened patients, 149 patients with sepsis and stage 1 or 2 AKI were included, in which 63 patients developed progressive AKI and 49 patients subsequently died during hospitalization. u[TIMP-2][IGFBP7], uKIM-1 and uIL-18 independently predicted the progression of septic AKI in which u[TIMP-2][IGFBP7] showed the greatest AUC (0.745; 95%CI, 0.667-0.823) as compared to uKIM-1 (AUC 0.719; 95%CI 0.638-0.800) and uIL-18 (AUC 0.619; 95%CI 0.525-0.731). Combination of u[TIMP-2][IGFBP7] with uKIM-1 improved the performance of predicting septic AKI progression with AUC of 0.752. u[TIMP-2][IGFBP7], alone or combined with uKIM-1/uIL-18, improved the risk reclassification over the clinical risk factor model alone both for the primary and secondary outcomes, as evidenced by significant category-free net reclassification index.
CONCLUSIONS
Combination of renal cell arrest and damage biomarkers enhanced the prediction of AKI progression in patients with sepsis and improved risk reclassification over the clinical risk factors.
背景
脓毒症是急性肾损伤（AKI）最常见的诱因，高达 40%的轻度或中度脓毒症 AKI 会进展为更严重的 AKI，这与死亡风险和后期慢性肾脏病/终末期肾病（CKD/ESRD）显著增加相关。早期识别脓毒症 AKI 进展的高危患者是脓毒症 AKI 患者面临的主要挑战。
方法
这是一项前瞻性、多中心队列研究，纳入了 2014 年 1 月至 2018 年 3 月期间在重症监护病房（ICU）中最初发生 1 期或 2 期 AKI 的脓毒症成年患者。AKI 根据 2012 年 KDIGO-AKI 指南进行诊断和分期。在 AKI 临床诊断时测量肾细胞阻滞生物标志物（尿 TIMP2IGFBP7，u[TIMP-2][IGFBP7]）和肾损伤生物标志物（尿 KIM-1[uKIM-1]和尿 IL-18 [uIL-18]），并评估生物标志物单独或联合预测脓毒症 AKI 进展的性能。主要结局为 AKI 进展，定义为 AKI 分期恶化。次要结局为住院期间 AKI 进展后继发死亡。
结果
在筛选的 433 名患者中，纳入了 149 名患有脓毒症和 1 期或 2 期 AKI 的患者，其中 63 名患者出现 AKI 进展，49 名患者随后在住院期间死亡。u[TIMP-2][IGFBP7]、uKIM-1 和 uIL-18 均可独立预测脓毒症 AKI 的进展，其中 u[TIMP-2][IGFBP7]的 AUC（0.745；95%CI，0.667-0.823）最大，而 uKIM-1（AUC 0.719；95%CI，0.638-0.800）和 uIL-18（AUC 0.619；95%CI，0.525-0.731）。u[TIMP-2][IGFBP7]联合 uKIM-1 可提高预测脓毒症 AKI 进展的性能，AUC 为 0.752。u[TIMP-2][IGFBP7]单独或与 uKIM-1/uIL-18 联合使用，在主要和次要结局方面，均可提高临床危险因素模型的风险再分类，证据为类别自由净再分类指数显著增加。
结论
肾细胞阻滞和损伤生物标志物的联合使用可提高脓毒症患者 AKI 进展的预测能力，并提高临床危险因素的风险再分类。
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