Objective:To compare the early diagnostic value of the indicators of endothelial injury, renal injury, inflammation and coagulation in patients with sepsis-induced acute kidney injury (AKI).Methods:A retrospective study was performed on 119 patients with sepsis from February 2017 to March 2018. Lab tests were performed on patients at admission, which included:ing soluble thrombomodulin (sTM), tissue plasminogen activators and inhibitors (t-PAI-C), antithrombin III (AT-III), thrombin-antithrombin (TAT) complex, plasmin-alpha 2, plasmin inhibitor complex (PIC), fibrin degradation product (FDP), fibrinogen (FIB), D-Dimer, prothrombin time (PT), prothrombin time international normalized ratio (PT-INR), procalcitoni (PCT), white blood cell (WBC), neutrophil (Neu), and platelet count (PLT). The receiver-operating characteristic curve was used to analyze the predictive value of the above indicators, and logistic regression analysis was used to analyze the risk factors of sepsis-induced AKI. A prospective study was conducted from April 2018 to September 2018 and 46 patients were enrolled. The lab tests results retrieved including sTM, t-PAI-C, FDP, AT-III, TAT, PIC, FIB, D-Dimer, PT, PCT, serum cystatin C (Cys C), urine albumin (microalbumin) and albumin to creatinine ratio (ACR), urinary neutrophil gelatinase-associated lipocalin (uNGAL), urinary N-acetyl-beta-glucosaminidase (uNAG), and urinary retinol-binding protein (uRBP). As same with the previous group, the receiver-operating characteristic curve was used to analyze the diagnostic value of the above indicators, and logistic regression Was used to analyze the risk factors of sepsis-induced AKI.Results:(1) In the retrospective study: sTM, D-Dimer, PCT, PT, and PT-INR were statistically different. sTM, D-Dimer, PCT, PT, and PT-INR had a good diagnostic value for septis-induced AKI, among which, sTM had a highest diagnostic value (AUC: 0.857; 95% CI: 0.790, 0.924), better sensitivity (64.4%) and specificity (91.8%). The high expression of sTM and history of chronic kidney disease were independent risk factors for septis-induced AKI.(2) In the prospective study: PCT, sTM , Cys C, and uNGAL were statistically different. PCT, sTM, Cys C, uNGAL showed good predictive features for septis-induced AKI. sTM had the highest sensitivity (>0.999) while uNGAL had the highest specificity (0.800). The high expression of sTM was an independent risk factor for septis-induced AKI. Conclusions:sTM and uNGAL represent endothelial injury and renal tubular injury respectively. sTM is an independent risk factor of sepsis-induced AKI.

Objective:To investigate the differential expression of cyclooxygenase (COX) gene between familial aggregated atherosclerotic large-artery atherosclerosis(LAA) cerebral infarction patients and sporadic LAA cerebral infarction patients.Methods:Twenty-five patients with familial aggregation LAA cerebral infarction (familial aggregation LAA group) and 25 sporadic LAA cerebral infarction patients (sporadic LAA group) were collected.Another 25 patients with non-cardiovascular and cerebrovascular diseases were selected as control group.Real-time quantitative PCR and ELISA were used to detect COX-1 and COX-2 protein in the supernatant of samples.Results:The expression level of COX-1 gene was 0.5436±0.2737, 0.2400±0.1656 and 0.8340±0.3799 in the familial aggregation, sporadic LAA cerebral infarction and control groups.Compared with control group, COX-1 gene expression in sporadic LAA cerebral infarction group and familial aggregation LAA cerebral infarction group was significantly down-regulated, the differences were significant( P<0.05). The expression level of COX-2 gene was 1.3672±0.8249, 1.3932±0.7158 and 0.7212±0.9623 in the familial aggregation, sporadic LAA cerebral infarction and control groups.Compared with the normal control group, the expression of COX-2 gene in familial aggregation LAA cerebral infarction group and sporadic LAA cerebral infarction group increased significantly( P<0.05). The expression of COX-1 protein was 2.9956±0.5672, 2.5572±1.0289 and 2.6721±0.7944 in the familial aggregation, sporadic cerebral infarction and control groups.The expression of COX-2 protein was 16.63±4.06, 16.86±7.93 and 15.94±5.94 in the familial aggregation, sporadic cerebral infarction and control groups.There was no significant difference in the relative expression of COX-1 and COX-2 proteins among familial aggregation LAA cerebral infarction group, sporadic LAA cerebral infarction group and control group(all P>0.05). Conclusion:There is significant difference in COX-1 gene expression between patients with familial LAA and sporadic LAA cerebral infarction.