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Objective: The objective of this study was to assess the relationship between serum procalcitonin (PCT) and acute kidney injury (AKI) induced by bacterial septic shock. Methods: A retrospective study was designed which included patients who were admitted to the ICU from January 2015 to October 2018. Multiple logistic regression and receiver operating characteristic (ROC) as well as smooth curve fitting analysis were used to assess the relationship between the PCT level and AKI. Results: Of the 1,631 patients screened, 157 patients were included in the primary analysis in which 84 (53.5%) patients were with AKI. Multiple logistic regression results showed that PCT (odds ratio [OR] = 1.017, 95% confidence interval [CI] 1.009–1.025, p < 0.001) was associated with AKI induced by septic shock. The ROC analysis showed that the cutoff point for PCT to predict AKI development was 14 ng/mL, with a sensitivity of 63% and specificity 67%. Specifically, in multivariate piecewise linear regression, the occurrence of AKI decreased with the elevation of PCT when PCT was between 25 ng/mL and 120 ng/mL (OR 0.963, 95% CI 0.929–0.999; p = 0.042). The AKI increased with the elevation of PCT when PCT was either p = 0.006) or >120 ng/mL (OR 1.042, 95% CI 1.009–1.076; p = 0.013). Moreover, the PCT level was significantly higher in the AKI group only in female patients aged ≤75 years (p = 0.001). Conclusions: Our data revealed a nonlinear relationship between PCT and AKI in septic shock patients, and PCT could be used as a potential biomarker of AKI in female patients younger than 75 years with bacterial septic shock.

Objective This study aims to assess the relationship between serum procalcitonin (PCT) and acute kidney injury (AKI) induced by sepsis shock.Methods A case-control study was designed which included patients that admitted in intensive care unit (ICU) between January 2015 and October 2018. The worst values of biochemical parameters in the first 48 hours from septic shock admission to ICU were evaluated. According to KDIGO guideline, these patients were divided into AKI and non-AKI groups.Results Of 1631 patients screened, 157 patients were included in the primary analysis in which 84 (53.5%) patients with AKI. Multiple logistic regression results showed that PCT (OR=1.017, 95% CI 1.009- 1.025, P

MicroRNA-132 (miR-132) is correlated with inflammatory response regulation, although its effect on acute kidney injury to provide protection against hemorrhagic shock remains currently unknown. AChE in macrophages of the kidney subjected under hemorrhagic shock is presumed to be regulated by miR-132 after its transcription to alleviate the inflammatory response accordingly. Antagonists such as acetylcholine (Ach) (concentration 10−4mol/L) and galanthamine (Gal) (concentration 10μmol/L) were added into separate groups 1 hour after the macrophages in the kidney were isolated and cultured to induce injury under oxygen and glucose deprivation (OGD) and then cultured for 24 hours. To analyze the effect of miR-132, we placed the renal epithelial cells transfected with miR-132 plasmids with stable expression over the renal macrophages to create a double cell culture system. The expression levels of inflammatory factors and apoptosis under OGD were significantly higher in renal macrophages than in other experimental groups. Moreover, the expression of miR-132 in macrophages of the double cell culture system showing stable expression of miR-132 increased, whereas that of several inflammatory factors was significantly inhibited. The expression levels of AChE mRNA and protein in the macrophages significantly decreased. The cholinergic antiinflammatory pathway in renal macrophages is regulated by miR-132 via inhibition of the hydrolytic activity of cholinesterase to alleviate inflammatory response, which may play a role in the prevention and treatment of kidney injury caused by hemorrhagic shock.

Objective To investigate the effects of cholinergic pathway on acute renal tubular cell injury induced by acute oxygen and glucose deprivation. Methods Rat kidney macrophages were isolated and cultured for constructing macrophages and renal epithelial cells co-cultivating model of oxygen-glucose deprivation (OGD), and the model cells were divided into three groups: OGD alone group, acetylcholine (ACh 100μmol/L)+OGD group and ACh + galantamine (Gal 10μmol/L)+OGD group. The cells underwent OGD treatment for 1 hour, and normally cultured for 24 hours. The expressions of TNF alpha, IL-1 beta, and IL-10 in supernatant fluid were detected by ELISA, the renal tubular cell viability was determined by MTT assay, the expression of acetylcholine esterase (AChE) mRNA and protein were determined by RT-qPCR and Western blotting. The activity of AChE was determined by colorimetric method. Results The expressions of TNF alpha (pg/ml) in OGD, Ach+OGD group, Ach+Gal+OGD groups were 140.2±44.81, 119.46±4.42 and 103.31±1.62 respectively (P0.05); The values of renal tubular cell proliferation were 55.02%±6.28%, 66.65%±6.47%, and 79.75%±4.22% respectively (P0.05); those of AchE protein were 0.66±0.07, 0.74±0.04 and 0.67±0.06 respectively (P>0.05); The activity of AChE (kU/L) was 0.51±0.02, 0.35±0.05 and 0.32±0.04 respectively (P=0.001, 0.001 and 0.368). Conclusions ACh and Gal could inhibit the secretion of inflammatory mediators and cholinesterase activity and can reduce the acute hypoxic renal tubular cell injury. The modulation of the cholinergic pathway in macrophages may be the important treatment method for acute renal injury in the future. DOI: 10.11855/j.issn.0577-7402.2017.08.01