Objective:To explore the diagnostic value of serum solute carrier family 7 member 11 (SLC7A11), urinary retinol-binding protein (RBP) and transferrin (TRF) for acute kidney injury (AKI) in patients with sepsis.Methods:The clinical data of 204 patients with sepsis from January 2020 to December 2023 in the Second Affiliated Hospital of Xi′an Medical College were retrospectively analyzed. Among them, 102 patients complicated with AKI (AKI group), including Kidney Disease: Improving Global Outcomes (KDIGO) classification Ⅰ stage 43 cases, Ⅱ stage 36 cases, Ⅲ stage 23 cases; 102 patients did not complicate with AKI (non-AKI group). Additionally, 102 healthy individuals from the same period were selected as a healthy control group. Enzyme-linked immunosorbent assay was used to detect the serum expression level of SLC7A11, and fully automatic biochemical analyzers were used to detect urinary RBP and TRF levels. For patients in AKI group and non-AKI group, the sequential organ failure assessment (SOFA) was recorded; fully automatic analyzers were used to test hematological indicators, including creatinine, hemoglobin, platelet, albumin, uric acid, lactate, procalcitonin and C-reactive protein, and estimated glomerular filtration rate (eGFR) was calculated. Multivariate Logistic regression analysis was used to analyze the independent risk factors of AKI in patients with sepsis. Receiver operating characteristic (ROC) curve was plotted to analyze the values of serum SLC7A11 and urinary RBP, TRF in assessing the risk of AKI in patients with sepsis.Results:The serum SLC7A11 and urinary RBP, TRF in non-AKI group and AKI group were significantly higher than those in healthy control group: (28.66 ± 6.22) and (36.18 ± 7.29) ng/L vs. (14.32 ± 2.63) ng/L, (1.20 ± 0.25) and (1.47 ± 0.31) mg/L vs. (0.44 ± 0.08) mg/L, (1.82 ± 0.39) and (2.26 ± 0.45) mg/L vs. (1.08 ± 0.19) mg/L, furthermore the indexes in AKI group were significantly higher than those in non-AKI group, and there were statistical differences ( P<0.05). The serum SLC7A11 and urinary RBP, TRF in patients with KDIGO Ⅱ stage and Ⅲ stage were significantly higher than those in patients with KDIGO Ⅰ stage: (37.16 ± 7.41) and (45.20 ± 8.29) ng/L vs. (30.53 ± 6.46) ng/L, (1.50 ± 0.28) and (1.72 ± 0.35) mg/L vs. (1.31 ± 0.26) mg/L, (2.26 ± 0.46) and (2.77 ± 0.59) mg/L vs. (1.99 ± 0.40) mg/L, furthermore the indexes in patients with KDIGO Ⅲ stage were significantly higher than those in patients with KDIGO Ⅱ stage, and there were statistical differences ( P<0.05). The SOFA, creatinine and lactate in AKI group were significantly higher than those in non-AKI group: 12 (9, 15) scores vs. 7 (5, 9) scores, (133.71 ± 13.58) μmol/L vs. (108.18 ± 14.32) μmol/L and (13.61 ± 3.57) mmol/L vs. (10.95 ± 3.10) mmol/L, the albumin and eGFR were significantly lower than those in non-AKI group: (21.48 ± 2.48) g/L vs. (24.85 ± 2.83) g/L and (51.57 ± 9.64) ml/(min·1.73 m 2) vs. (59.21 ± 10.67) ml/(min·1.73 m 2), and there were statistical differences ( P<0.01); there were no statistical differences in hemoglobin, platelet, uric acid, procalcitonin and C-reactive protein between two groups ( P>0.05). Multivariate Logistic regression analysis result showed that the high SOFA, creatinine, lactate, SLC7A11, urinary RBP, urinary TRF, and low eGFR, albumin were independent risk factors for AKI in patients with sepsis ( OR = 4.864, 5.631, 2.315, 5.862, 6.852, 6.218, 0.328 and 0.226; 95% CI 1.701 to 13.907, 1.803 to 17.585, 1.350 to 3.969, 2.115 to 16.242, 2.177 to 21.566, 1.900 to 20.353, 0.151 to 0.713 and 0.092 to 0.555; P<0.01). The ROC curve analysis result showed that the area under the curve of the combined assessment of serum SLC7A11 and urinary RBP, TRF for AKI in patients with sepsis was significantly larger than serum SLC7A11 and urinary RBP, TRF alone (0.892 vs. 0.774, 0.765 and 0.755), and there was statistical difference ( Z = 2.97, 3.20 and 3.38; P<0.01). Conclusions:The elevated expression levels of serum SLC7A11 and urinary RBP and TRF in patients with sepsis have a high value for the combined detection and assessment of AKI.

Objective:To explore the diagnostic value of serum solute carrier family 7 member 11 (SLC7A11), urinary retinol-binding protein (RBP) and transferrin (TRF) for acute kidney injury (AKI) in patients with sepsis.Methods:The clinical data of 204 patients with sepsis from January 2020 to December 2023 in the Second Affiliated Hospital of Xi′an Medical College were retrospectively analyzed. Among them, 102 patients complicated with AKI (AKI group), including Kidney Disease: Improving Global Outcomes (KDIGO) classification Ⅰ stage 43 cases, Ⅱ stage 36 cases, Ⅲ stage 23 cases; 102 patients did not complicate with AKI (non-AKI group). Additionally, 102 healthy individuals from the same period were selected as a healthy control group. Enzyme-linked immunosorbent assay was used to detect the serum expression level of SLC7A11, and fully automatic biochemical analyzers were used to detect urinary RBP and TRF levels. For patients in AKI group and non-AKI group, the sequential organ failure assessment (SOFA) was recorded; fully automatic analyzers were used to test hematological indicators, including creatinine, hemoglobin, platelet, albumin, uric acid, lactate, procalcitonin and C-reactive protein, and estimated glomerular filtration rate (eGFR) was calculated. Multivariate Logistic regression analysis was used to analyze the independent risk factors of AKI in patients with sepsis. Receiver operating characteristic (ROC) curve was plotted to analyze the values of serum SLC7A11 and urinary RBP, TRF in assessing the risk of AKI in patients with sepsis.Results:The serum SLC7A11 and urinary RBP, TRF in non-AKI group and AKI group were significantly higher than those in healthy control group: (28.66 ± 6.22) and (36.18 ± 7.29) ng/L vs. (14.32 ± 2.63) ng/L, (1.20 ± 0.25) and (1.47 ± 0.31) mg/L vs. (0.44 ± 0.08) mg/L, (1.82 ± 0.39) and (2.26 ± 0.45) mg/L vs. (1.08 ± 0.19) mg/L, furthermore the indexes in AKI group were significantly higher than those in non-AKI group, and there were statistical differences ( P<0.05). The serum SLC7A11 and urinary RBP, TRF in patients with KDIGO Ⅱ stage and Ⅲ stage were significantly higher than those in patients with KDIGO Ⅰ stage: (37.16 ± 7.41) and (45.20 ± 8.29) ng/L vs. (30.53 ± 6.46) ng/L, (1.50 ± 0.28) and (1.72 ± 0.35) mg/L vs. (1.31 ± 0.26) mg/L, (2.26 ± 0.46) and (2.77 ± 0.59) mg/L vs. (1.99 ± 0.40) mg/L, furthermore the indexes in patients with KDIGO Ⅲ stage were significantly higher than those in patients with KDIGO Ⅱ stage, and there were statistical differences ( P<0.05). The SOFA, creatinine and lactate in AKI group were significantly higher than those in non-AKI group: 12 (9, 15) scores vs. 7 (5, 9) scores, (133.71 ± 13.58) μmol/L vs. (108.18 ± 14.32) μmol/L and (13.61 ± 3.57) mmol/L vs. (10.95 ± 3.10) mmol/L, the albumin and eGFR were significantly lower than those in non-AKI group: (21.48 ± 2.48) g/L vs. (24.85 ± 2.83) g/L and (51.57 ± 9.64) ml/(min·1.73 m 2) vs. (59.21 ± 10.67) ml/(min·1.73 m 2), and there were statistical differences ( P<0.01); there were no statistical differences in hemoglobin, platelet, uric acid, procalcitonin and C-reactive protein between two groups ( P>0.05). Multivariate Logistic regression analysis result showed that the high SOFA, creatinine, lactate, SLC7A11, urinary RBP, urinary TRF, and low eGFR, albumin were independent risk factors for AKI in patients with sepsis ( OR = 4.864, 5.631, 2.315, 5.862, 6.852, 6.218, 0.328 and 0.226; 95% CI 1.701 to 13.907, 1.803 to 17.585, 1.350 to 3.969, 2.115 to 16.242, 2.177 to 21.566, 1.900 to 20.353, 0.151 to 0.713 and 0.092 to 0.555; P<0.01). The ROC curve analysis result showed that the area under the curve of the combined assessment of serum SLC7A11 and urinary RBP, TRF for AKI in patients with sepsis was significantly larger than serum SLC7A11 and urinary RBP, TRF alone (0.892 vs. 0.774, 0.765 and 0.755), and there was statistical difference ( Z = 2.97, 3.20 and 3.38; P<0.01). Conclusions:The elevated expression levels of serum SLC7A11 and urinary RBP and TRF in patients with sepsis have a high value for the combined detection and assessment of AKI.

Methods To investigate how the timing of cooling therapy affects organ injuries in rats with exertional heat stroke(EHS)and explore the possible mechanisms.Methods A total of 60 adult male Wistar rat models of EHS were randomized into model group without active cooling after modeling,immediate cooling group with cold water bath immediately after modeling,delayed cooling groups with cold water bath at 5,15 and 30 min after modeling,with another 12 mice without EHS as the normal control group.The changes in core body temperature of the mice were recorded and the cooling rate was calculated.After observation for 24 h,the mice were euthanized and blood samples were collected for detection of interleukin-1β(IL-1β),IL-2,IL-4,IL-6,IL-10,and interferon-γ,followed by pathological examination of the vital organs.The rats that died within 24 h were immediately dissected for examination.Results The number of deaths of the model rats within 24 h increased significantly with the time of delay of cooling treatment.The delay of cooling was positively correlated(r=0.996,P=0.004)while the cooling rate negatively correlated with the mortality rate(r=-0.961,P=0.009).The inflammatory cytokine levels presented with different patterns of variations among the cooling intervention groups.All the rat models of EHS had significant organ damages characterized mainly by epithelial shedding,edema,effusion,and inflammatory cell infiltration,and brain and renal injuries reached the peak level at 24 h after EHS.Conclusion EHS causes significant nonspecific pathologies of varying severities in the vital organs of rats,and the injuries worsen progressively with the delay of cooling.There is a significant heterogeneity in changes of serum inflammatory cytokines in rats with different timing of cooling intervention following EHS.

Methods To investigate how the timing of cooling therapy affects organ injuries in rats with exertional heat stroke(EHS)and explore the possible mechanisms.Methods A total of 60 adult male Wistar rat models of EHS were randomized into model group without active cooling after modeling,immediate cooling group with cold water bath immediately after modeling,delayed cooling groups with cold water bath at 5,15 and 30 min after modeling,with another 12 mice without EHS as the normal control group.The changes in core body temperature of the mice were recorded and the cooling rate was calculated.After observation for 24 h,the mice were euthanized and blood samples were collected for detection of interleukin-1β(IL-1β),IL-2,IL-4,IL-6,IL-10,and interferon-γ,followed by pathological examination of the vital organs.The rats that died within 24 h were immediately dissected for examination.Results The number of deaths of the model rats within 24 h increased significantly with the time of delay of cooling treatment.The delay of cooling was positively correlated(r=0.996,P=0.004)while the cooling rate negatively correlated with the mortality rate(r=-0.961,P=0.009).The inflammatory cytokine levels presented with different patterns of variations among the cooling intervention groups.All the rat models of EHS had significant organ damages characterized mainly by epithelial shedding,edema,effusion,and inflammatory cell infiltration,and brain and renal injuries reached the peak level at 24 h after EHS.Conclusion EHS causes significant nonspecific pathologies of varying severities in the vital organs of rats,and the injuries worsen progressively with the delay of cooling.There is a significant heterogeneity in changes of serum inflammatory cytokines in rats with different timing of cooling intervention following EHS.