ObjectiveTo analyze the etiological characteristics and risk factors of autosomal dominant polycystic kidney disease （ADPKD） complicated with urinary tract infection （UTI）. MethodsA retrospective analysis was performed on 244 patients with ADPKD admitted to the Department of Nephrology. The patients were stratified into a study group （n=138） and a control group （n=106） according to the presence or absence of concurrent UTI. All patients in the study group underwent etiological testing and drug susceptibility testing. Clinical data of both groups were collected to identify the risk factors for ADPKD complicated with UTI. ResultsA total of 105 pathogens were detected in 138 cases in the study group， including 79 Gram-negative bacteria， 20 Gram-positive bacteria and 6 fungi. Escherichia coli showed a relatively high resistance rate to ampicillin， piperacillin and ciprofloxacin. Enterococcus faecalis had a relatively high resistance rate to tetracycline. There were statistically significant differences between the study group and the control group in terms of gender， history of urinary tract infection， C-reactive protein （CRP）， increased urine red blood cells， increased urine white blood cells， increased percentage of neutrophils， blood sodium， blood calcium， total cholesterol， serum iron and transferrin saturation （P<0.05）. Multivariate binary Logistic regression analysis revealed that female gender （OR=2.236， P=0.004）， history of urinary tract infection （OR=2.383， P=0.002）， increased urine white blood cells （OR=2.726， P=0.001）， increased percentage of neutrophils （OR=1.040， P=0.010）， elevated C-reactive protein （OR=1.011， P=0.007） and elevated blood calcium （OR=4.389， P=0.024） were risk factors of urinary tract infection in ADPKD patients （P<0.05）. ConclusionThe main pathogens of UTI in patients with ADPKD are Gram-negative bacteria. Female， previous history of urinary tract infection， urinary leukocytosis， increased percentage of neutrophils， increased CRP and increased serum calcium are risk factors of UTI.

Objective To elucidate the regulatory effects of Glycerol Kinase(GLPK)on the inflammatory response induced by lipopolysaccharide(LPS)in mouse Raw264.7 macrophages.Methods Raw264.7 macrophages were cultured in vitro,and an inflammatory model was established through LPS induction.The transcriptional levels of inflammatory cytokines NF-κB,TNF-α,IL-6,and IL-1β were quantified using RT-qPCR.The expression and localization of GLPK were examined via Western blot and immunofluorescence.Additionally,Western blot analysis was employed to detect the levels of cellular pan-succinylation and H3K23su expression.ChIP-qPCR was utilized to assess the enrichment of H3K23su modification at the IL-10 promoter.The total reactive oxygen species production was measured using DCFH-DA probes,while mitochondrial ROS levels were determined with Mito-SOX probes.Mitochondrial membrane potential changes,indicative of mitochondrial dysfunction,were evaluated using JC-1 fluorescent probes.Furthermore,GLPK overexpression plasmids were transfected into cells to investigate the effects of GLPK on inflammatory responses,mitochondrial function,and epigenetic modifications.Results LPS treatment led to mitochondrial dysfunction,inflammatory responses exacerbation,succinylation modifications reduction,and GLPK protein expression decrease in Raw264.7 cells.Overexpression of GLPK in LPS-treated cells improved mitochondrial function and reduced the transcription of pro-inflammatory cytokines.ChIP-qPCR analysis revealed that GLPK overexpression could reverse the LPS-induced suppression of H3K23su modification at the IL-10 promoter,thereby attenuating the inflammatory response.Conclusion LPS mediates inflammatory responses in Raw264.7 macrophages through a GLPK-dependent H3K23 succinylation modification mechanism.

Objective To elucidate the regulatory effects of Glycerol Kinase(GLPK)on the inflammatory response induced by lipopolysaccharide(LPS)in mouse Raw264.7 macrophages.Methods Raw264.7 macrophages were cultured in vitro,and an inflammatory model was established through LPS induction.The transcriptional levels of inflammatory cytokines NF-κB,TNF-α,IL-6,and IL-1β were quantified using RT-qPCR.The expression and localization of GLPK were examined via Western blot and immunofluorescence.Additionally,Western blot analysis was employed to detect the levels of cellular pan-succinylation and H3K23su expression.ChIP-qPCR was utilized to assess the enrichment of H3K23su modification at the IL-10 promoter.The total reactive oxygen species production was measured using DCFH-DA probes,while mitochondrial ROS levels were determined with Mito-SOX probes.Mitochondrial membrane potential changes,indicative of mitochondrial dysfunction,were evaluated using JC-1 fluorescent probes.Furthermore,GLPK overexpression plasmids were transfected into cells to investigate the effects of GLPK on inflammatory responses,mitochondrial function,and epigenetic modifications.Results LPS treatment led to mitochondrial dysfunction,inflammatory responses exacerbation,succinylation modifications reduction,and GLPK protein expression decrease in Raw264.7 cells.Overexpression of GLPK in LPS-treated cells improved mitochondrial function and reduced the transcription of pro-inflammatory cytokines.ChIP-qPCR analysis revealed that GLPK overexpression could reverse the LPS-induced suppression of H3K23su modification at the IL-10 promoter,thereby attenuating the inflammatory response.Conclusion LPS mediates inflammatory responses in Raw264.7 macrophages through a GLPK-dependent H3K23 succinylation modification mechanism.