Costa Nara Aline, Gut Ana Lúcia, Azevedo Paula Schmidt, Tanni Suzana Erico, Cunha Natália Baraldi, Magalhães Eloá Siqueira, Silva Graziela Biude, Polegato Bertha Furlan, Zornoff Leonardo Antonio Mamede, de Paiva Sergio Alberto Rupp, Balbi André Luís, Ponce Daniela, Minicucci Marcos Ferreira
Department of Internal Medicine, Botucatu Medical School, UNESP - Univ Estadual Paulista, Rubião Júnior s/n, Botucatu, SP, CEP: 18618-970, Brazil.
Department of Food and Experimental Nutrition, Faculty of Pharmaceutical Science, University of São Paulo, São Paulo, SP, Brazil.
Ann Intensive Care. 2016 Dec;6(1):95. doi: 10.1186/s13613-016-0198-5. Epub 2016 Oct 6.
Oxidative stress is a key feature of sepsis and could be a common pathophysiological pathway between septic shock and acute kidney injury (AKI) Our objective was to evaluate the erythrocyte superoxide dismutase (SOD1) activity as predictor of AKI in patients with septic shock.
This is a prospective observational study that evaluated 175 consecutive patients over the age of 18 years with septic shock upon intensive care unit (ICU) admission. However, 43 patients were excluded (27 due to AKI at ICU admission). Thus, 132 patients were enrolled in the study. At the time of the patients' enrollment, demographic information was recorded. Blood samples were taken within the first 24 h of the patient's admission to determine the erythrocyte SOD1 activity. All patients were followed throughout the ICU stay, and the development of AKI was evaluated. In addition, we also evaluated 17 control subjects.
The mean age of patients with septic shock was 63.2 ± 15.7 years, 53 % were male and the median ICU stay was 8 days (4-16). Approximately 50.7 % developed AKI during the ICU stay. The median erythrocyte SOD1 activity was 2.92 (2.19-3.92) U/mg Hb. When compared to control subjects, septic shock patients had a higher serum malondialdehyde concentration and lower erythrocyte SOD1 activity. In univariate analysis, erythrocyte SOD1 activity was lower in patients who developed AKI. The ROC curve analysis revealed that lower erythrocyte SOD1 activity was associated with AKI development (AUC 0.686; CI 95 % 0.595-0.777; p < 0.001) at the cutoff of <3.32 U/mg Hb. In the logistic regression models, SOD1 activity higher than 3.32 U/mg Hb was associated with protection of AKI development when adjusted by hemoglobin, phosphorus and APACHE II score (OR 0.309; CI 95 % 0.137-0.695; p = 0.005) and when adjusted by age, gender, chronic kidney disease, admission category (medical or surgery) and APACHE II score (OR 0.129; CI 95 % 0.033-0.508; p = 0.003).
In conclusion, our data suggest that erythrocyte SOD1 activity could play a role as an early marker of septic AKI and could be seen as a new research avenue in the field of biomarker in AKI. However, our study did not show a strong correlation between SOD activity and AKI. Nevertheless, these original data do warrant further research in order to confirm or not this hypothesis.
氧化应激是脓毒症的关键特征，可能是脓毒性休克与急性肾损伤（AKI）之间的共同病理生理途径。我们的目的是评估红细胞超氧化物歧化酶（SOD1）活性作为脓毒性休克患者发生AKI的预测指标。
这是一项前瞻性观察性研究，评估了175例年龄在18岁以上、入住重症监护病房（ICU）时患有脓毒性休克的连续患者。然而，43例患者被排除（27例因入住ICU时已发生AKI）。因此，132例患者纳入研究。在患者入组时，记录人口统计学信息。在患者入院后的头24小时内采集血样以测定红细胞SOD1活性。对所有患者在整个ICU住院期间进行随访，并评估AKI的发生情况。此外，我们还评估了17名对照受试者。
脓毒性休克患者的平均年龄为63.2±15.7岁，53%为男性，ICU住院时间中位数为8天（4 - 16天）。在ICU住院期间，约50.7%的患者发生了AKI。红细胞SOD1活性中位数为2.92（2.19 - 3.92）U/mg Hb。与对照受试者相比，脓毒性休克患者的血清丙二醛浓度更高，红细胞SOD活性更低。在单因素分析中，发生AKI的患者红细胞SOD1活性较低。ROC曲线分析显示，红细胞SOD1活性降低与AKI的发生相关（AUC 0.686；95%CI 0.595 - 0.777；p<0.001），截断值为<3.32 U/mg Hb。在逻辑回归模型中，当通过血红蛋白、磷和APACHE II评分进行校正时，SOD1活性高于3.32 U/mg Hb与预防AKI的发生相关（OR 0.309；95%CI 0.137 - 0.695；p = 0.005）；当通过年龄、性别、慢性肾脏病、入院类别（内科或外科）和APACHE II评分进行校正时，也与之相关（OR 0.129；95%CI 0.033 - 0.508；p = 0.003）。
总之，我们的数据表明红细胞SOD1活性可能作为脓毒症性AKI的早期标志物发挥作用，并且可被视为AKI生物标志物领域的一个新的研究方向。然而，我们的研究并未显示SOD活性与AKI之间有很强的相关性。尽管如此，这些原始数据确实值得进一步研究以证实或否定这一假设。
