[Bioinformatics analysis and validation of key genes in transformation of idiopathic membranous nephropathy to end-stage renal disease and traditional Chinese medicines for prevention and treatment].

This study used bioinformatics analysis to screen out key genes involved in the transformation of idiopathic membranous nephropathy to end-stage renal disease and to predict targeted Chinese herbs and medicines and active ingredients with preventive and curative effects. The GSE108113 microarray of idiopathic membranous nephropathy and GSE37171 microarray of were downloaded from the comprehensive gene expression database, and 8 homozygous differentially expressed genes for the transformation of idiopathic membranous nephropathy into end-stage renal disease of were screened out by R software. GraphPad Prism was used to verify the expression of homozygous differentially expressed genes in GSE115857 microarray of idiopathic membranous nephropathy and GSE66494 microarray of chronic kidney disease, and 7 key genes(FOS, OGT, CLK1, TIA1, TTC14, CHORDC1, and ANKRD36B) were finally obtained. The Gene Ontology(GO) analysis was performed. There were 209 functions of encoded proteins, mainly involved in regulation of RNA splicing, cytoplasmic stress granule, poly(A) binding, etc. Thirteen traditional Chinese medicines with the effect of preventing the transformation of idiopathic membranous nephropathy to end-stage renal disease were screened out from Coremine Medical database, including Ginseng Radix et Rhizoma, Lycopi Herba, and Gardeniae Fructus, which were included in the Chinese Pharmacopoeia(2020 edition). The active ingredient quercetin mined from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP) had ability to dock with the key gene FOS-encoded protein molecule, which provided targets and research ideas for the development of new traditional Chinese medicines.

Association between interleukin 8-receptor gene (CXCR1 and CXCR2) polymorphisms and urinary tract infection: Evidence from 4097 subjects.

AIM: The aim of this study was to determine whether a correlation exists between interleukin-8 receptor polymorphisms and urinary tract infection (UTI) susceptibility. METHODS: We systematically searched electronic databases including PubMed, Embase, China National Knowledge Infrastructure, and Web of Science up to 5 November 2017 to select appropriate studies that focused on C-X-C chemokine receptor type 1 and/or 2 (CXCR1, CXCR2) polymorphisms with susceptibility to UTI. Eight case-control studies including 2085 patients with UTI and 2012 controls were enrolled in this study. Seven studies of CXCR1 rs2234671 and two studies of rs3138086 were included in the meta-analyses. Pooled odds ratio (OR) and corresponding 95% confidence interval (CI) were synthesized using fixed-effects or random-effects model according to heterogeneity. RESULTS: No significant correlations were found between CXCR1 rs2234671 and rs3138086 polymorphisms and UTI susceptibility. However, subgroup analysis showed that rs2234671 was associated with an increased risk of UTI under allelic comparisons (C vs. G, OR = 1.95, 95% CI = 1.07-3.55), heterozygous model (GC vs. GG, OR = 1.93, 95% CI = 1.06-3.50), and dominant model (GC + CC vs. GG, OR = 1.98, 95% CI = 1.07-3.69) in children, especially in paediatric patients with acute pyelonephritis (allelic, OR = 2.43, 95% CI = 1.28-4.60; heterozygous, OR = 2.40, 95% CI = 1.24-4.62; dominant, OR = 2.48, 95% CI = 1.26-4.88). Furthermore, these results remained the same after eliminating paediatric patients with vesicoureteral reflux. CONCLUSION: CXCR1 rs2234671 polymorphism might be associated with an increased risk of UTI in children.

A PRISMA-compliant meta-analysis of MDR1 polymorphisms and idiopathic nephrotic syndrome: Susceptibility and steroid responsiveness.

BACKGROUND: Studies have investigated rs1128503, rs1045642, and rs2032582 in multidrug resistance protein 1 (MDR1) for association with susceptibility to idiopathic nephrotic syndrome (INS) and steroid resistance. However, because these findings were inconsistent, we performed a meta-analysis to determine whether there was evidence of a role of these MDR1 variants in INS. METHODS: The PubMed, Embase, and Web of Science databases were systematically searched to identify studies that examined MDR1 polymorphisms with susceptibility to INS and/or to steroid resistance. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by a fixed-effects or random-effects model based on heterogeneity. RESULTS: We selected 9 case-control studies that included 928 patients with INS, of which steroid resistance data were available for 724 (236 were steroid resistant and 488 were steroid sensitive), and 879 healthy controls. All subjects were children. No significant relationships between these polymorphisms and INS susceptibility were identified. Significantly increased risk of steroid resistance was observed with rs1128503 allelic (OR = 1.49, 95% CI = 1.20-1.86) and genotypic (OR = 1.97, 95% CI = 1.18-3.30; OR = 2.03, 95% CI = 1.43-2.88) comparisons, and with allelic (OR = 1.56, 95% CI = 1.05-2.31) and genotypic (OR = 2.85, 95% CI = 1.15-7.07; OR = 2.21, 95% CI = 1.01-4.8) comparisons to rs2032582 in Caucasian populations. However, this association between rs2032582 and steroid resistance was not robust enough to withstand corrections for multiple comparisons. Similarly, we found that the rs1128503T-rs2032582G-rs1045642C (T-G-C) haplotype was associated with an increased risk of steroid resistance (OR = 2.02, 95% CI = 1.13-3.59), while the wild-type C-G-C haplotype was associated with a decreased risk (OR = 0.32, 95% CI = 0.12-0.88) in Caucasians; however, these findings were not significant following adjustments for multiple comparisons. CONCLUSIONS: MDR1 rs1128503, rs1045642, and rs2032582 polymorphisms are not associated with INS susceptibility; however, there is evidence of an association between rs1128503 and increased risk of steroid resistance in children with INS, which indicates MDR1 may play a role in steroid resistance found in children with INS.