Combining renal cell arrest and damage biomarkers to predict progressive AKI in patient with sepsis.
Combining renal cell arrest and damage biomarkers to predict progressive AKI in patient with sepsis.
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联合肾细胞停滞和损伤生物标志物预测脓毒症患者的进展性阿基
DOI：
10.1186/s12882-021-02611-8
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发表时间：
2021-12-15
期刊：
影响因子：
2.3
通讯作者：
Hou FF
中科院分区：
文献类型：
--
作者：
Tao X;Chen C;Luo W;Zhou J;Tian J;Yang X;Hou FF
脓毒症是阿基最常见的触发因素，高达40%的轻度或中度脓毒阿基会进展为更严重的阿基，这与死亡和晚期CKD/ESRD的风险显著增加相关。早期识别阿基进展的高风险患者是脓毒性阿基患者的主要挑战。这是一项前瞻性、多中心队列研究，入组了2014年1月至2018年3月期间在重症监护室最初发生1期或2期阿基的脓毒症成人患者。根据2012年KDIGO-AKI指南对阿基进行诊断和分期。在阿基临床诊断时测量肾细胞停滞生物标志物（尿TIMP 2 * IGFBP 7，u[TIMP-2]*[IGFBP 7]）和肾损伤生物标志物（尿KIM-1[uKIM-1]和尿IL-18 [uIL-18]），并评价生物标志物单独或联合用于预测脓毒性阿基进展的性能。主要结局为阿基进展，定义为阿基分期恶化。次要结局为阿基进展，随后在住院期间死亡。在433例筛选的患者中，纳入了149例脓毒症和1期或2期阿基患者，其中63例患者发生进展性阿基，49例患者随后在住院期间死亡。u[TIMP-2]*[IGFBP 7]、uKIM-1和uIL-18独立预测脓毒性阿基的进展，其中u[TIMP-2]*[IGFBP 7]显示最大AUC（0.745; 95%CI，0.667-0.823），与uKIM-1（AUC 0.719; 95%CI 0.638-0.800）和uIL-18（AUC 0.619; 95%CI 0.525-0.731）相比。u[TIMP-2]*[IGFBP 7]与uKIM-1的组合改善了预测脓毒性阿基进展的性能，AUC为0.752。u[TIMP-2]*[IGFBP 7]单独或与uKIM-1/uIL-18组合，对于主要和次要结局，相对于单独的临床风险因素模型改善了风险重新分类，如显著的无类别净重新分类指数所证明的。肾细胞停滞和损伤生物标志物的组合增强了脓毒症患者阿基进展的预测，并改善了临床风险因素的风险重新分类。在线版本包含补充材料，可通过10.1186/s12882-021-02611-8获得。
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. 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 TIMP2*IGFBP7, 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. 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. 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. The online version contains supplementary material available at 10.1186/s12882-021-02611-8.
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影响因子：
13.6
作者：
Koyner, Jay L.;Garg, Amit X.;Parikh, Chirag R.
通讯作者：
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影响因子：
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作者：
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作者：
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通讯作者：
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影响因子：
8.8
作者：
Angus, D C;Linde-Zwirble, W T;Pinsky, M R
通讯作者：
Pinsky, M R
影响因子：
39.2
作者：
Levey AS;Stevens LA;Schmid CH;Zhang YL;Castro AF 3rd;Feldman HI;Kusek JW;Eggers P;Van Lente F;Greene T;Coresh J;CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration)
通讯作者：
CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration)