炎性体相关细胞因子在脓毒症急性肾损伤中的变化和意义

Inflammasome-regulated cytokines in sepsis-induced acute kidney injury

目的：观察炎性体相关细胞因子在脓毒症急性肾损伤（AKI）患者中的变化情况，探讨其价值及意义。方法选择2014-03-2015-02哈尔滨医科大学附属一院ICU收治的非脓毒症非AKI患者29例作为ICU control组，脓毒症非AKI患者30例作为Sepsis not AKI组，脓毒症AKI患者34例作为Sepsis-induced AKI组，于患者入ICU第1天、3天和7天取血并收集清晨中段尿液，采用酶联免疫吸附试验（ELISA）检测血浆和尿液中IL-1β、IL-18和IL-33，计算急性生理学与慢性健康状况评分系统Ⅱ（APACHEⅡ）评分；同时记录ICU住院时间、血清肌酐（SCr）水平和每天的尿量。计数资料使用χ^2检验，计量资料使用两组间比较采用两独立样本t检验，多组间比较采用单因素方差分析。结果与ICU control组比较，Sepsis not AKI组APACHEⅡ评分、SCr水平、尿量和住ICU时间均无显著变化（均P＞0.05）；Sepsis-induced AKI组患者的APACHEⅡ评分、SCr水平显著升高（P＜0.05），尿量显著减少（P＜0.05），住ICU时间显著延长（P＜0.05）。在第1天、3天和7天， Sepsis not AKI组患者和Sepsis-induced AKI组患者的血浆IL-1β、IL-18和IL-33水平均比同时间点ICU control组患者显著升高（均P＜0.05），而Sepsis-induced AKI组患者的IL-1β、IL-18和IL-33血浆水平均高于同时间点Sepsis not AKI组患者（均P＜0.05）；Sepsis-induced AKI组患者的尿IL-1β、IL-18和IL-33水平均高于同时间点的ICU control组和Sepsis not AKI组患者（均P＜0.05），而ICU control组和Sepsis not AKI组患者同时间点的尿细胞因子水平差异无统计学意义（均P＞0.05）。结论炎性体相关因子在脓毒症AKI患者中是上调表达的，炎性体的活化可能在脓毒症AKI的形成中起了重要作用。

Objective To investigate the inflammasome-regulated cytokines in sepsis-induced acute kidney injury（AKI）patients, and to explore their value and significance. Methods Twenty-nine non-septic patients with no AKI（ICU control group）, 30 septic patients with no AKI（Sepsis not AKI group）and 34 patients with septic AKI（Sepsis-induced AKI group）in intensive care unit（ICU）of the First Affiliated Hospital of Harbin Medical University were enrolled in this study. On the 1st, 3rd and 7th day, blood and urine samples were collected, IL-1β, IL-18 and IL-33 levels in plasma and urine were measured using enzyme-linked immunosorbent assay （ELISA）. Acute physiology and chronic health evaluation Ⅱ（APACHE Ⅱ）score was calculated, while the ICU stay, serum creatinine levels and urine output were recorded. Chi-square test, unpaired t test and one-way analysis of variance（ANOVA）were used for statistical analysis. Results Compared with the ICU control group, APACHE Ⅱscore and serum creatinine（SCr）were significantly increased, the urine output was markedly decreased and the duration of ICU stay was significantly longer in the Sepsis-induced AKI group but not in the Sepsis not AKI group. On the 1st, 3rd and 7th day, compared with the ICU control group, plasma and urine levels of IL-1β, IL-18 and IL-33 were significantly elevated in the Sepsis-induced AKI group on the same time point, plasma levels but not urine levels of IL-1β, IL-18 and IL-33 were markedly increased in the Sepsis not AKI group. Compared with the Sepsis not AKI group, plasma and urine levels of IL-1β, IL-18 and IL-33 were significantly increased in the Sepsis-induced AKI group on the same time point. Conclusion The inflammasome-regulated cytokines are upregulated in patients with septic AKI. Inflammasome activation may play an important role in the formation of septic AKI.