INTRODUCTION A major complication of sepsis is the development of acute kidney injury (AKI). Recently, it was shown that intracellular actin released from damaged tissues appears in the urine of patients with multiple organ dysfunction syndrome. Our aims were to measure urinary actin (u-actin) concentrations of septic and control patients and to test if u-actin levels could predict AKI and mortality. METHODS Blood and urine samples were collected from septic and sepsis-related AKI patients at three time points (T1-3): T1: within 24 hours after admission; T2: second day morning; T3: third day morning of follow-up. Patients with malignancies needing palliative care, end-stage renal disease or kidney transplantation were excluded. Serum and u-actin levels were determined by quantitative Western blot. Patients were categorized by the Sepsis-3 and KDIGO AKI classifications. RESULTS In our study, 17 septic, 43 sepsis-induced AKI and 24 control patients were enrolled. U-actin levels were higher in septic patients compared with controls during follow-up (p<0.001). At T1, the septic and sepsis-related AKI groups also showed differences (p<0.001), yet this increase was not statistically significant at T2 and T3. We also detected significantly elevated u-actin concentrations in AKI-2 and AKI-3 septic patients compared with AKI-1 septic patients (p<0.05) at T1 and T3, along with a significant increase in AKI-2 septic patients compared with AKI-1 septic patients at T2 (p<0.01). This tendency remained the same when referring u-actin to urine creatinine. Parameters of first-day septic patient samples could discriminate AKI from non-AKI state (AUC ROC, p<0.001): u-actin: 0.876; se-creatinine: 0.875. Derived cut-off value for u-actin was 2.63 μg/L (sensitivity: 86.0%, specificity: 82.4%). CONCLUSION U-actin may be a complementary diagnostic biomarker to se-creatinine in sepsis-related AKI while higher u-actin levels also seem to reflect the severity of AKI. Further investigations may elucidate the importance of u-actin release in sepsis-related AKI.

中文翻译：

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尿肌动蛋白，作为脓毒症相关急性肾损伤的潜在标志物：一项初步研究。

引言 败血症的一个主要并发症是急性肾损伤 (AKI) 的发展。最近有研究表明，多器官功能障碍综合征患者的尿液中出现了受损组织释放的细胞内肌动蛋白。我们的目标是测量脓毒症患者和对照患者的尿肌动蛋白 (u-actin) 浓度，并测试 u-actin 水平是否可以预测 AKI 和死亡率。方法 在三个时间点（T1-3）采集脓毒症和脓毒症相关 AKI 患者的血液和尿液样本： T1：入院后 24 小时内；T2：第二天早上；T3：随访的第三天上午。需要姑息治疗、终末期肾病或肾移植的恶性肿瘤患者被排除在外。通过定量蛋白质印迹确定血清和 u-肌动蛋白水平。患者按照 Sepsis-3 和 KDIGO AKI 分类进行分类。结果 在我们的研究中，17 名脓毒症患者、43 名脓毒症诱发的 AKI 患者和 24 名对照患者入选。在随访期间，脓毒症患者的 U-肌动蛋白水平高于对照组（p<0.001）。在 T1 时，脓毒症和脓毒症相关 AKI 组也显示出差异（p<0.001），但这种增加在 T2 和 T3 时没有统计学意义。我们还在 T1 和 T3 检测到 AKI-2 和 AKI-3 脓毒症患者的 u-actin 浓度显着高于 AKI-1 脓毒症患者（p<0.05），同时 AKI-2 脓毒症患者与 AKI 相比显着增加-1 名 T2 脓毒症患者 (p<0.01)。当将 u-actin 称为尿肌酐时，这种趋势保持不变。脓毒症患者第一天样本的参数可以将 AKI 与非 AKI 状态区分开来（AUC ROC，p<0.001）：u-肌动蛋白：0.876；肌酐：0.875。u-肌动蛋白的衍生截断值为 2.63 μg/L（灵敏度：86.0%，特异性：82.4%）。结论 U-肌动蛋白可能是脓毒症相关 AKI 中 se-肌酐的补充诊断生物标志物，而较高的 u-肌动蛋白水平似乎也反映了 AKI 的严重程度。进一步的研究可能会阐明 u-肌动蛋白释放在脓毒症相关 AKI 中的重要性。