Background: This study was conducted to evaluate and update the current prevalence of and risk factors for chronic kidney disease (CKD) and diabetic kidney disease (DKD) in a central Chinese urban population. Methods: From December 2017 to June 2018, a total of 5231 subjects were randomly enrolled from 3 communities in 3 districts of Zhengzhou. CKD was defined as estimated glomerular filtration rate (eGFR) < 60 mL/min.1.73m 2 or urinary albumin to creatinine ratio ≥ 30 mg/g (albuminuria). Diabetic subjects with systolic blood pressure > 140 mmHg, albuminuria or an eGFR less than 60 mL/min/1.73 m 2 were classified as having DKD. Participants completed a questionnaire assessing lifestyle and relevant medical history, and blood and urine specimens were taken. Serum creatinine, uric acid, total cholesterol, triglycerides, low-density lipoprotein, high-density lipoprotein and urinary albumin were assessed. The age-and sex-adjusted prevalences of CKD and DKD were calculated, and risk factors associated with the presence of reduced eGFR, albuminuria, DKD, severity of albuminuria and progression of reduced renal function were analyzed by binary and ordinal logistic regression. Results: The overall adjusted prevalence of CKD was 16.8% (15.8-17.8%) and that of DKD was 3.5% (3.0-4.0%). Decreased renal function was detected in 132 participants (2.9, 95% confidence interval [CI]: 2.5-3.2%), whereas albuminuria was found in 858 participants (14.9, 95% CI: 13.9-15.9%). In all participants with diabetes, the prevalence of reduced eGFR was 6.3% (95% CI = 3.9-8.6%) and that of albuminuria was 45.3% (95% CI = 40.4-50.1%). The overall prevalence of CKD in participants with diabetes was 48.0% (95% CI = 43.1-52.9%). The results of the binary and ordinal logistic regression indicated that the factors independently associated with a higher risk of reduced eGFR and albuminuria were older age, sex, smoking, alcohol consumption, overweight, obesity, diabetes, hypertension, dyslipidemia and hyperuricemia.

The antimicrobial resistance and the character of integrons were determined in 58 Shigella flexneri strains isolated from China. All isolates were multi-drug resistant and found to carry integrons of class 1 (94.8%), class 2 (100%), or both (94.8%). No intI3 was detected. The typical class 1 integrons were found in conjugative plasmids and could be transferred to the recipient E. coli DH5α. The gene cassettes of typical class 1 integrons dfrA17-aadA5 and dfrA12-orfF-aadA2 were detected in 54 strains (93.1%) and 1 strain, respectively. Atypical class 1 integrons located on the chromosome with gene cassettes bla (oxa-30)-aadA1 were detected in 55 isolates (94.8%). All the intI2 positive isolates carried gene cassettes dfrA1-sat1-aadA1. To our knowledge, this is the first report that atypical and typical class 1 integrons coexisted with class 2 integron in multi-drug resistant S. flexneri strains.

IceA of Helicobacter pylori (H. pylori) has been suggested as a virulence factor for the bacteria, but its pathogenic role remains unelucidated. Here, we examined the effect of iceA mutation on the secretion of IL-8 by human gastric epithelial cells. We also investigated whether the changes in IL-8 production caused by iceA mutation were associated with impaired adherence of H. pylori to the epithelial cells or with impaired apoptosis of these cells. The iceA mutant strain was constructed from wildtype H. pylori strain by insertional mutagenesis of iceA. The human gastric epithelial cells SGC7901 were infected with wildtype or mutant H. pylori for appropriate lengths of time. The adherence of the bacteria to the epithelial cells was examined by fluorescent microscopy using an anti-H. pylori antibody and flow cytometry. The apoptosis of the epithelial cells was studied by annexin-V staining and flow cytometry. The production of IL-8 by SGC 7901 cells was determined by ELISA. We found that iceA mutation was associated with significantly impaired production of IL-8 from the epithelial cells, which was not due to impaired adherence by the bacteria to the epithelial cells as wildtype and mutant H. pylori exhibited similar levels of binding to the epithelial cells. Furthermore, inactivation of iceA did not affect the apoptotic cell death of SGC7901. Our findings indicate that iceA may contribute to the pathogenicity of H. pylori by modulating the production of IL-8 by host epithelial cells.