BackgroundEmerging evidence indicates that gut dysbiosis is involved in the occurrence and development of diabetic kidney diseases (DKD). However, the key microbial taxa closely related to DKD have not been determined.MethodsPubMed, Web of Science, Cochrane, Chinese Biomedical Databases, China National Knowledge Internet, and Embase were searched for case-control or cross-sectional studies comparing the gut microbiota of patients with DKD and healthy controls (HC) from inception to February 8, 2022, and random/fixed-effects meta-analysis on the standardized mean difference (SMD) were performed for alpha diversity indexes between DKD and HC, and beta diversity indexes and the relative abundance of gut microbiota were extracted and summarized qualitatively.ResultsA total of 16 studies (578 patients with DKD and 444 HC) were included. Compared to HC, the bacterial richness of patients with DKD was significantly decreased, and the diversity indexes were decreased but not statistically, companying with a distinct beta diversity. The relative abundance of phylum Proteobacteria, Actinobacteria, and Bacteroidetes, family Coriobacteriaceae, Enterobacteriaceae, and Veillonellaceae, genus Enterococcus, Citrobacter, Escherichia, Klebsiella, Akkermansia, Sutterella, and Acinetobacter, and species E. coli were enriched while that of phylum Firmicutes, family Lachnospiraceae, genus Roseburia, Prevotella, and Bifidobacterium were depleted in patients with DKD.ConclusionsThe gut microbiota of patients with DKD may possess specific features characterized by expansion of genus Escherichia, Citrobacter, and Klebsiella, and depletion of Roseburia, which may contribute most to the alterations of their corresponding family and phylum taxa, as well as the bacterial diversity and composition. These microbial taxa may be closely related to DKD and serve as promising targets for the management of DKD.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD42021289863.
BackgroundGut dysbiosis is postulated to participate in the pathogenesis of IgA nephropathy (IgAN). However, the key bacterial taxa closely associated with IgAN onset and treatment response have not been identified.MethodsWe recruited 127 patients with IgAN who were treatment naive and 127 matched healthy controls (HCs) who were randomly divided into discovery and validation cohorts to investigate the characteristics of their gut microbiota and establish a bacterial diagnosis model for IgAN. A separate cohort of 56 patients and HCs was investigated to assess crossregional validation. A further 40 patients with primary membranous nephropathy (MN) were enrolled to probe disease-specific validation. A subgroup of 77 patients was prospectively followed to further dissect the association between alterations in gut microbiota and treatment response after 6 months of immunosuppressive therapy. Fecal microbiota samples were collected from all participants and analyzed using 16S ribosomal RNA sequencing.ResultsDecreased α-diversity (Shannon, P=0.03), altered microbial composition (Adonis, P=0.0001), and a striking expansion of the taxonomic chain Proteobacteria–Gammaproteobacteria–Enterobacteriales–Enterobacteriaceae–Escherichia-Shigella (all P<0.001) were observed in patients with IgAN who were treatment naive, which reversed only in patients who achieved clinical remission after 6 months of immunosuppressive therapy. Importantly, seven operational taxa units, of which Escherichia-Shigella contributed the most, were determined to be the optimal bacterial classifier of IgAN (AUC=0.8635, 0.8551, 0.8026 in discovery, validation, and cross-regional validation sets, respectively), but did not effectively distinguish patients with IgAN versus those with MN (AUC=0.6183). Bacterial function prediction further verified enrichment of the shigellosis infection pathway in IgAN.ConclusionGut dysbiosis, characterized by a striking expansion of genus Escherichia-Shigella, is a hallmark of patients with IgAN and may serve as a promising diagnostic biomarker and therapeutic target for IgAN. Further studies are warranted to investigate the potential contribution of Escherichia-Shigella in IgAN pathogenesis.
BackgroundProbiotics, prebiotics, and synbiotics are three different supplements to treat end stage renal disease (ESRD) patients by targeting gut bacteria. The comprehensive comparison of the effectiveness of different supplements are lacking.ObjectivesThe purpose of this network meta-analysis (NMA) is to assess and rank the efficacy of probiotics, prebiotics, and synbiotics on inflammatory factors, uremic toxins, and gastrointestinal symptoms (GI symptoms) in ESRD patients undergoing dialysis.MethodsRandomized clinical trials were searched from the PubMed, Embase, and Cochrane Register of Controlled Trials databases, from their inception until 4 September 2021. Random-effect model were used to obtain all estimated outcomes in network meta-analysis (NMA). Effect estimates were presented as mean differences (Mean ± SD) with 95% confidence interval (CI). The comprehensive effects of all treatments were ranked by the surface under the cumulative ranking (SUCRA) probabilities.ResultsTwenty-five studies involved 1,106 participants were included. Prebiotics were superior in decreasing Interleukin-6 (IL-6; SMD –0.74, 95% CI [–1.32, –0.16]) and tumor-necrosis factor-α (TNF-α; SMD –0.59, 95% CI [–1.09, –0.08]), synbiotics were more effective in declining C-reactive protein (CRP; SMD –0.69, 95% CI [–1.14, –0.24]) and endotoxin (SMD –0.83, 95% CI [–1.38, –0.27]). Regarding uremic toxins, prebiotics ranked highest in reducing indoxyl sulfate (IS; SMD –0.43, 95% CI [–0.81, –0.05]), blood urea nitrogen (BUN; SMD –0.42, 95% CI [–0.78, –0.06]), and malondialdehyde (MDA; SMD –1.88, 95% CI [–3.02, –0.75]). Probiotics were rated as best in alleviating GI symptoms (SMD: –0.52, 95% CI [–0.93, –0.1]).ConclusionOur research indicated prebiotics were more effective in declining IL-6, TNF-α, IS, MDA, and BUN, synbiotics lowering CRP and endotoxin significantly, and probiotics were beneficial for alleviating GI symptoms, which may contribute to better clinical decisions. This study was registered in PROSPERO (Number: CRD42021277056).Systematic Review Registration[http://www.crd.york.ac.uk/PROSPERO], identifier [CRD42021277056].
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