Objectives To investigate the role and mechanism of p38 mitogerra activated protein kinase (p38MAPK) in up-regulation of prostanoid 2 induced by uric acid in rat glomerular mesangial cells (GMCs).Methods Rat glomerular mesangial cells were cultured in vitro,then stimulated with different concentrations of uric acid (50,100,300 μmol/L),or stimulated with different concentrations of uric acid (50,100,300 μmol/L) after pretreatment with p38MAPK specific inhibitor SC68376 (10 μmol/L) for 30 min.Activated p38MAPK was detected by Western blotting.The expression of prostanoid 2 was measured by ELISA.Cyclooxygenase-2 mRNA expression was determined by RT-PCR.Results Uric acid could activate p38MAPK and up-regulate the mRNA expressions of prostanoid 2 and cyclooxygenase-2 in rat glomerular mesangial cells (all P ＜ 0.05).SC68376 inhibited those effects of the above-described induced by uric acid.Conclusion Uric acid can promote the expression of prostanoid 2 in rat glomerular mesangial cells,whose mechanism may be related to the activation of p38MAPK and the promotion of cyclooxygenase-2 synthesis,and further up-regulation of prostanoid 2 expression.

Objective:To explore the predictive value of complement and coagulation indicators in sepsis related acute kidney injury (AKI).Methods:Clinical data of 217 patients with sepsis admitted to the Department of Internal Medicine and Intensive Care Unit of Affiliated Hospital of Jiangnan University from January 2018 to June 2019 were retrospectively analyzed. All patients were divided into sepsis with AKI group and without AKI group. Laboratory indicators of all patients were collected, including complement C 3, complement C 4, activated partial thrombin time (APTT), prothrombin time (PT), international normalized ratio (INR), D-dimer, procalcitonin(PCT), etc. logistic regression analysis was used to explore the risk factors of sepsis related AKI. Receiver operating characteristic curve (ROC) was used to evaluate the predictive value of independent risk factors. Results:Among 217 patients, 120 patients developed sepsis related AKI and 97 patients didn′t. PCT, lactic acid, PT, APTT, INR and D-dimer in AKI patients were significantly higher than those without AKI ( P<0.01). Complement C 3 and complement C 4 were significantly lower in AKI group ( P<0.01). Multivariate logistic regression analysis suggested that blood pressure<90/60 mmHg (1 mmHg=0.133 kPa)( OR=3.705, 95% CI 1.536-8.934, P=0.004), increased lactic acid ( OR=1.479, 95% CI 1.089-2.008, P=0.012), decreased complement C 3 ( OR=0.027, 95% CI 0.005-0.152, P<0.001) and prolonged APTT ( OR=1.090, 95% CI 1.047-1.137, P<0.001)were independent risk factors predicting AKI. The area under the ROC curve (AUC) of these multivariates were 0.741 (95% CI 0.675-0.807), 0.798 (95% CI 0.732-0.864), 0.712 (95% CI 0.643-0.781) and 0.716 (95% CI 0.648-0.783) respectively. The relevant sensitivity was 57.5%, 80.8%, 87.5%, 59.2%, and the specificity was 90.7%, 75.3%, 51.5%, 77.3%, respectively. The AUC of the combined four indicators was 0.880 (95 %CI 0.835-0.926) with the sensitivity 75.0% and the specificity 90.7%. Conclusion:The low level of complement C 3 and prolonged APTT predict sepsis related AKI, and the predictive value can be enhanced if hypotension and hyperlactacidemia are added.