AIM:To explore the effect of Toll-like receptor ( TLR) 2 and TLR4 in Mycobacterium bovis Bacil-lus Calmette-Guérin (BCG)-induced human proximal renal tubule epithelial cell (HK-2) injury.METHODS:HK-2 cells were stimulated by BCG, and the expression of TLR2, TLR4, chemokine (C-X3-C motif) ligand 1 (CX3CL1) and trans-forming growth factor beta 1 ( TGF-β1 ) was detected by quantitative real-time PCR and Western blotting .TLR2 monoclonal antibody and TLR4 inhibitor were used to treat the HK-2 cells 1 h before BCG stimulation.The expression of CX3CL1 and TGF-β1 was evaluated by quantitative real-time PCR and Western blotting .RESULTS: BCG increased the expression of TLR2, TLR4, CX3CL1 and TGF-β1 in the HK-2 cells.Additionally, the expression of CX3CL1 and TGF-β1 was inhibited partly by TLR2 monoclonal antibody or TLR4 inhibitor.CONCLUSION:BCG is able to increase the production of TLR 2, TLR4, CX3CL1 and TGF-β1 in the HK-2 cells.TLR2 and TLR4 signaling pathways play important roles in tubule epitheli-al cell injury induced by BCG .

Objective To study the occurrence site characteristics of middle cerebral artery aneurysm (MCAA ) in volume CT digital subtraction angiograhy(VCTDSA) .Methods The image characteristics in 72 cases of MCAA from May 2009 to January 2011 were retrospectively analyzed ,according to the running of middle cerebral artery ,the occurrence sites of aneurysm were divided into four categories :M1 segment ,M2 bifurcation ,M2 distal and M3-M5 segment ,the aneurysm number was conducted the statistics and the image characteristics were analyzed ;two neuroradiologists adopted the double-blind method to measure the MCAA angle in bifurcation of M2 segment and compared it with the bifurcation angle in the normal middle cerebral artery ,the difference between them were statistically analyzed .Results (1)M1 segment aneurysms were 7 cases(9 .70% ) ,M2 bifurcation aneurysms were 58 ca-ses(80 .56% ) ,M2 distal aneurysms were 5 cases(6 .94% ) and M3-M5 segment aneurysms were 2 cases(2 .78% ) .(2)The angle in M2 bifurcation of the normal middle cerebral artery was(99 .30 ± 22 .96)° ,M2 bifurcation aneurysm angle was(139 .26 ± 27 .61)° , the difference between them showing statistical significance (P<0 .01) .(3)The difference between left and right of M 2 bifurcation angle in the normal middle cerebral artery had no statistical significance (P>0 .05) .(4)The M2 bifurcation angle in ruptured aneu-rysm was(133 .98 ± 30 .24)° ,which in unruptured aneurysms was(144 .53 ± 21 .81)° ,the difference between them had no statistical significance(P>0 .05) .Conclusion MCAA mainly occurred in M2 bifurcation .There is significant difference in M2 bifurcation an-gle between the aneurysm group and non-aneurysm group ,M2 bifurcation angle is increased ,the probability of aneurysm occurrence is increased .

Objective To investigate the impact of preoperative hyperuricemia on acute kidney injury (AKI) after cardiac surgery with cardiopulmonary bypass (CPB).Methods A total of 567 adult patients undergoing cardiac surgery with CPB were enrolled to conduct a retrospective cohort database analysis.The patients were divided into hyperuricemia group and non-hyperuricemia group according to preoperative serum uric acid,and the incidence of AKI in two groups were compared.Binary logistic regression analysis was used to evaluate the relationship between preoperative hyperuricemia and AKI.Results Among 567 patients after cardiac surgery with CPB,hyperuricemia occurred in 303 cases (53.4％),and AKI occurred in 217 cases (38.3％).There was significantdifference in the incidence of AKI between hyperuricemia group and non-hyperuricemia group (44.6％ vs 31.1％,x2=10.874,P=0.001).The duration of intensive care unit (ICU) stay and the length of stay were longer in hyperuricemia group than those in non-hyperuricemia group (both P ＜ 0.05).After adjusting for age,gender,comorbidities (hypertension,diabetes mellitus,cerebrovascular disease),preoperative renal function,preoperative heart function,CPB time,intraoperative aortic block time,type of cardiac surgery and postoperative hypotension,binary logistic regression analysis showed that preoperative hyperuricemia was an independent risk factor of AKI after cardiac surgery with CPB (OR=1.912,95％ CI 1.270-2.879,P=0.002).Conclusion AKI is a common complication following cardiac surgery with CPB,and hyperuricemia is independently associated with CPB-associated AKI.Hyperuricemia may be involved in the pathogenesis of AKI,and intervention before cardiac surgery may be beneficial to prevent postoperative AKI.

Objective:To investigate the effect of hyperuricemia on acute kidney injury in sepsis patients.Methods:It is a retrospective cohort study of 459 adult sepsis patients who were admitted to the Department of Intensive Care Unit (ICU) of the First Affiliated Hospital of Guangxi Medical University from March 2014 to June 2019, and the Second Affiliated Hospital of Guangxi Medical University from January 2017 to June 2019. The patients were divided into the hyperuricemia group and the non-hyperuricemia group according to the first serum uric acid level within 24 h after ICU admission, and the incidence of AKI within 7 days after ICU admission was compared between the two groups. The effect of hyperuricemia on sepsis-associated AKI was analyzed by univariate analysis and binary logistic regression analysis.Results:Among the 459 sepsis patients, 81 patients (17.6%) had hyperuricemia, and 127 patients (27.7%) had AKI. The incidence of AKI in the hyperuricemia group and the non-hyperuricemia group were 60.5% (49/81) and 20.6% (78/378), respectively, which showed significantly statistical difference ( χ2=52.954, P<0.01). After adjusting for gender, associated diseases (diabetes, coronary heart disease), sequential organ failure score (SOFA) on the day of ICU admission, the use of diuretics within one week before and after ICU admission, invasive mechanical ventilation, basal renal function, lactic acid, and procalcitonin, binary logistic regression analysis showed that hyperuricemia was an independent risk factor for AKI in sepsis patients ( OR=5.091, 95% CI: 2.768-9.362, P<0.01); For every 1 mg/dL increase in serum uric acid in sepsis patients, the risk of developing AKI increased by 28.4% ( OR=1.284, 95% CI: 1.165-1.414, P<0.01). Conclusions:AKI is a common complication in sepsis patients admitted to ICU, and hyperuricemia is an independent risk factor for AKI in sepsis patients.

Objective:To explore the effect of serum lactic acid (Lac) level on acute kidney injury (AKI) in patients with sepsis and whether Lac level affects the in-hospital mortality of patients with sepsis-associated AKI.Methods:A retrospective cohort study was conducted. Clinical data of patients with sepsis admitted to the internal intensive care unit (ICU) of the First Affiliated Hospital of Guangxi Medical University from March 2014 to June 2019 and the ICU of the Second Affiliated Hospital of Guangxi Medical University from January 2017 to June 2020 were collected. According to the first quartile of Lac within 24 hours of admission to ICU, the patients were divided into Lac ≤ 1.4 mmol/L group (group Q1), Lac 1.5-2.4 mmol/L group (group Q2), Lac 2.5-4.0 mmol/L group (group Q3), and Lac ≥ 4.1 mmol/L group (group Q4). The incidence of sepsis-associated AKI after admission to ICU and hospital mortality were compared among four groups. The effect of elevated Lac on the incidence and mortality of sepsis-associated AKI was investigated by binary Logistic regression analysis. The receiver operator characteristic curve (ROC curve) was drawn to analyze the predictive value of Lac on the incidence and mortality of sepsis-associated AKI, and the cut-off value was obtained to analyze the incidence and death risk of sepsis-associated AKI at different Lac levels. Results:A total of 655 sepsis patients were enrolled, of which 330 patients (50.4%) developed AKI and 325 patients (49.6%) did not. Among 330 patients with sepsis-associated AKI, 134 (40.6%) died and 196 (59.4%) survived. With the increase of Lac level, the incidence of sepsis-associated AKI increased gradually (34.5%, 41.0%, 58.4%, 66.3%, respectively, in group Q1- Q4), meanwhile, the in-hospital mortality also increased gradually (23.4%, 29.2%, 33.1%, 43.4%, respectively, in group Q1- Q4), the differences were statistically significant (both P < 0.01). Compared with the non-AKI group, the Lac level in the AKI group was significantly increased [mmol/L: 3.08 (1.84, 5.70) vs. 1.91 (1.20, 3.10), P < 0.01]. After adjustment for factors such as gender (male), site of infection (abdominal cavity), vasoactive drugs, basal mechanical ventilation, mean arterial pressure (MAP), basal renal insufficiency, uric acid, procalcitonin (PCT), platelet count (PLT), basal serum creatinine (SCr) and basal estimated glomerular filtration rate (eGFR), and other influencing factors, multivariate Logistic regression analysis showed that elevated Lac was an independent risk factor for sepsis-associated AKI [odds ratio ( OR) = 1.096, 95% confidence interval (95% CI) was 1.022-1.175, P = 0.010]. Compared with the survival group, the Lac level in the death group was significantly increased [mmol/L: 3.55 (2.00, 6.76) vs. 3.00 (1.70, 4.50), P < 0.01]. After adjusting for age, diabetes, vasoactive drugs, basal eGFR, and other factors, multivariate Logistic regression analysis suggested that increased Lac was an independent risk factor for in-hospital mortality in sepsis-associated AKI patients ( OR = 1.074, 95% CI was 1.004-1.149, P = 0.037). ROC curve analysis showed that the area under the ROC curve (AUC) of Lac for predicting the incidence and mortality of sepsis-associated AKI was 0.653 (95% CI was 0.611-0.694) and 0.593 (95% CI was 0.530-0.656, both P < 0.01), respectively, and the cut-off values were 2.75 mmol/L (sensitivity was 57.8%, specificity was 69.2%) and 5.95 mmol/L (sensitivity was 56.7%, specificity was 83.7%). When the Lac ≥ 2.75 mmol/L, the risk of sepsis-associated AKI was 2.772 times higher than that of < 2.75 mmol/L ( OR = 2.772, 95% CI was 1.754-4.380, P < 0.001). When the Lac ≥ 5.95 mmol/L, the patients with sepsis-associated AKI had a 2.511 times higher risk of in-hospital death than those with Lac < 5.95 mmol/L ( OR = 2.511, 95% CI was 1.378-4.574, P = 0.003). Conclusions:Elevated Lac level is an independent risk factor for the incidence and mortality of sepsis-associated AKI. When Lac ≥ 2.75 mmol/L, the risk of AKI in patients with sepsis increased by 1.772 times; when Lac ≥ 5.95 mmol/L, the risk of in-hospital death in patients with sepsis related AKI increased by 1.511 times.

Objective:To investigate the effect of postoperative hypoalbuminemia on acute kidney injury (AKI) after cardiac surgery under cardiopulmonary bypass (CPB).Methods:The clinical data of adult patients undergoing cardiac surgery under CPB were retrospectively analyzed. The difference between preoperative and postoperative serum albumin level was compared. The patients were divided into hypoalbuminemia group (≤35 g/L) and non-hypoalbuminemia group (>35 g/L) according to the lowest serum albumin concentration within 48 hours after surgery. The incidence and severity of postoperative AKI were compared between the two groups. Univariate analysis and binary logistic regression analysis were used to evaluate the effect of postoperative hypoalbuminemia on the incidence of postoperative AKI.Results:Among the 749 patients, the serum albumin level after cardiac surgery was significantly lower than that before surgery ( Z=-15.739, P<0.001), and the proportion of patients with hypoalbuminemia increased from 9.6% to 27.6% ( χ2=83.516, P<0.001). Postoperative AKI occurred in 273 patients, including 109 cases (52.7%) in hypoalbuminemia group and 164 cases (30.3%) in non-hypoalbuminemia group. The incidence of AKI in hypoalbuminemia group was significantly higher than that in non-hypoalbuminemia group ( χ2=32.443, P<0.001), and the severity of AKI in hypoalbuminemia group increased than that in non-hypoalbuminemia group ( Z=-2.098, P=0.036), and the time of hospital stay extended ( Z=-2.442, P=0.015). After adjusted by gender, age, preoperative hypoalbuminemia, comorbidities (hypertension, hyperuricemia, diabetes mellitus, cerebrovascular disease), renal insufficiency, preoperative heart function, coronary angiography, CPB time, aorta blocking time, type of heart surgery and postoperative hypotension, binary logistic regression analysis revealed that postoperative hypoalbuminemia was an independent risk factor for CPB-associated AKI ( OR=2.319, 95% CI 1.586-3.392, P<0.001). Conclusions:AKI is a common complication following cardiac surgery under CPB. Serum albumin after CBP is significantly lower than that before CBP, and postoperative hypoalbuminemia within 48 hours after surgery is an independent risk factor for AKI.