Heme oxygenase-1 as a predictor of sepsis-induced acute kidney injury: a cross-sectional study.
Heme oxygenase-1 as a predictor of sepsis-induced acute kidney injury: a cross-sectional study.
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DOI：
10.21037/atm-22-4793
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发表时间：
2022-11
影响因子：
--
通讯作者：
Li, Nan
中科院分区：
文献类型：
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作者：
Xia, Shilin;Zhang, Meishuai;Liu, Han;Dong, Haibin;Wu, Nannan;Wiedermann, Christian J;Andaluz-Ojeda, David;Chen, Huiqing;Li, Nan
脓毒症患者炎症严重，预后不良。脓毒症引起的氧化应激和局部炎症可引发器官损伤，包括急性肾损伤（AKI）。既往研究表明，氧化应激下血红素加氧酶-1（HO-1）在近端肾小管细胞中过度表达，具有显着的细胞保护和抗炎作用。血红素加氧酶-1 (HO-1) 的组织表达增加可以拮抗脓毒症中血红素诱导的炎症，从而影响 AKI 的发生。研究人员在四种不同的 AKI 模型中观察到肾内 HO-1 表达以及血浆和尿液 HO-1 蛋白浓度的相应潜在增加。由于血清 HO-1 水平反映了 HO-1 表达，因此我们旨在研究血清 HO-1 是否可以预测脓毒症患者 AKI 的发生。本研究共纳入 83 例脓毒症患者，包括合并 AKI 的脓毒症患者和未合并 AKI 的脓毒症患者。根据脓毒症休克的定义和《肾脏疾病：改善全球结局》(KDIGO) 中描述的全球肾脏诊断标准，将患者分别分为脓毒症组和脓毒症休克组，伴有和不伴有 AKI。通过酶联免疫吸附测定（ELISA）测定血清HO-1水平。使用SPSS软件进行统计分析。脓毒症合并AKI患者与脓毒症无AKI患者在序贯器官衰竭评估（SOFA）评分、住院时间以及血清HO-1、肌酸激酶MB（CK-MB）、肌钙蛋白I（TnI）、尿素、肌红蛋白（MYO）、血清肌酐（Scr）、降钙素原、活化部分凝血活酶时间等实验室指标方面差异有统计学意义。碱性磷酸酶（ALP）、尿素、MYO、Scr、降钙素原、活化部分凝血活酶时间和凝血酶原时间的血清水平在四组之间表现出显着差异。与无 AKI 的脓毒症患者相比，脓毒症诱发的 AKI 患者血清 HO-1 浓度较高。脓毒症休克诱发 AKI 的患者血清 HO-1 水平升高。血清 HO-1 与 Scr 联合的受试者工作特征 (ROC) 曲线下面积为 0.885 [95% 置信区间 (CI)：0.761–1.000]。血清HO-1与脓毒症诱发的AKI呈正相关。这些发现表明，血清 HO-1 的测量可能在脓毒症诱发的 AKI 中发挥诊断和预测作用。
Sepsis patients suffer from severe inflammation and poor prognosis. Oxidative stress and local inflammation that results from sepsis can trigger organ injury, including acute kidney injury (AKI). Previous studies have shown that heme oxygenase-1 (HO-1) is overexpressed in proximal tubular cells under oxidative stress and has significant cytoprotective and anti-inflammatory effects. Heme-induced inflammation in sepsis is antagonized by increased tissue expression of heme oxygenase-1 (HO-1), which impacts on AKI development. The investigators observed intrarenal HO-1 expression and corresponding potential increases in plasma and urinary HO-1 protein concentrations in four different AKI models. Since serum levels of HO-1 reflect HO-1 expression, we aimed to investigate whether serum HO-1 could predict the development of AKI in sepsis patient. A total of 83 sepsis patients were enrolled in this study including septic patients with AKI and sepsis patients without AKI. According to the definition of septic shock and the global kidney diagnostic criteria described in the Kidney Disease: Improving Global Outcomes (KDIGO), patients were allocated to the sepsis and septic shock groups with and without AKI, respectively. The serum levels of HO-1 were measured by enzyme-linked immunosorbent assays (ELISA). Statistical analyses were performed using SPSS software. There were statistically significant differences between septic patients with AKI and sepsis patients without AKI in terms of Sequential Organ Failure Assessment (SOFA) score, hospitalization time, and laboratory indicators including serum HO-1, creatine kinase MB (CK-MB), troponin I (TnI), urea, myoglobin (MYO), serum creatinine (Scr), procalcitonin, and activated partial thromboplastin time. Serum levels of alkaline phosphatase (ALP), urea, MYO, Scr, procalcitonin, activated partial thromboplastin time, and prothrombin time exhibited significant differences among the four groups. The concentration of serum HO-1 was higher in sepsis-induced AKI compared with sepsis patients without AKI. Serum HO-1 levels were increased in patients with sepsis shock-induced AKI. The area under the receiver operating characteristic (ROC) curve for serum HO-1 combined with Scr was 0.885 [95% confidence interval (CI): 0.761–1.000]. Serum HO-1 is positively correlated with sepsis-induced AKI. These findings suggest that measurement of serum HO-1 may play a diagnostic and prediction role in sepsis-induced AKI.