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Phylogeny and differentially abundant gut microbiota taxa. A A maximum-likelihood phylogenetic tree of dereplicated genomes from the gut microbiota. The outermost grey bars represent the overall prevalence of the taxonomic bin. Orange and purple dots in the second layer denote taxonomic bins that were significantly more abundant in SF or HC, respectively (Benjamini–Hochberg corrected Wilcoxon test (P < 0.1) and effect size >|0.5|). Tree branches are coloured by phylum. B Average relative phylum abundance bar plot of HC and SF cohorts. Each vertical bar represents the average relative abundance within the cohort, coloured by phylum. C Effect sizes of taxa are coloured by cohort of enrichment and labelled where taxonomic information is available. Coloured species were significantly different by Benjamini–Hochberg corrected Wilcoxon test (P < 0.1) and effect size >|0.5|

Phylogeny and differentially abundant gut microbiota taxa. A A maximum-likelihood phylogenetic tree of dereplicated genomes from the gut microbiota. The outermost grey bars represent the overall prevalence of the taxonomic bin. Orange and purple dots in the second layer denote taxonomic bins that were significantly more abundant in SF or HC, respectively (Benjamini–Hochberg corrected Wilcoxon test (P < 0.1) and effect size >|0.5|). Tree branches are coloured by phylum. B Average relative phylum abundance bar plot of HC and SF cohorts. Each vertical bar represents the average relative abundance within the cohort, coloured by phylum. C Effect sizes of taxa are coloured by cohort of enrichment and labelled where taxonomic information is available. Coloured species were significantly different by Benjamini–Hochberg corrected Wilcoxon test (P < 0.1) and effect size >|0.5|

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Background Inquiry of microbiota involvement in kidney stone disease (KSD) has largely focussed on potential oxalate handling abilities by gut bacteria and the increased association with antibiotic exposure. By systematically comparing the gut, urinary, and oral microbiota of 83 stone formers (SF) and 30 healthy controls (HC), we provide a unified...

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... In a recent study, next-generation sequencing was utilized to examine 18 CaOx stones; the results showed that 7 stones contained bacterial 16S rRNA and human host nonribosomal DNA fragments, while fungal amplicon sequences were detected in 9 stones [19]. This identification of living microorganisms within the matrix of CaOx stones provides further evidence that the formation of kidney stones may occur through pathological biomineralization [25]. Pathological biomineraliza-tion of CaOx kidney stones arises from various microbial activities that affect the urinary supersaturation state, catalyze mineral precipitation, facilitate nucleation, and promote crystal growth and aggregation [5,21,25]. ...
... This identification of living microorganisms within the matrix of CaOx stones provides further evidence that the formation of kidney stones may occur through pathological biomineralization [25]. Pathological biomineraliza-tion of CaOx kidney stones arises from various microbial activities that affect the urinary supersaturation state, catalyze mineral precipitation, facilitate nucleation, and promote crystal growth and aggregation [5,21,25]. Several groups have suggested the existence of a kidney stone microbiome which may contribute to nephrolithiasis, while others have implicated the gut and urinary microbiomes [25,26]. nucleation, and promote crystal growth and aggregation [5,21,26]. ...
... Pathological biomineraliza-tion of CaOx kidney stones arises from various microbial activities that affect the urinary supersaturation state, catalyze mineral precipitation, facilitate nucleation, and promote crystal growth and aggregation [5,21,25]. Several groups have suggested the existence of a kidney stone microbiome which may contribute to nephrolithiasis, while others have implicated the gut and urinary microbiomes [25,26]. nucleation, and promote crystal growth and aggregation [5,21,26]. ...
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Kidney stone disease affects 12% of the global population with a prevalence that continues to increase. It is recurrent in up to 50% of patients within 5 years and is associated with major health concerns including coronary artery disease and chronic kidney disease. Thus, kidney stones pose a substantial health and economic burden. However, despite kidney stone disease being one of the oldest known and most common diseases worldwide, our understanding of the mechanisms underlying stone formation is lacking. Moreover, recent data have raised questions about the efficacy of currently used therapeutic options for calcium oxalate stones, which account for 75% of all kidney stones. Development of new therapeutics for the successful prevention and management of this disease will require improved understanding of the causes of kidney stones. Recent advancements have shed light on the nuanced contribution of diet, environment and genetics as well as the more fundamental roles of calcium oxalate crystallization, Randall’s plaque formation, inflammation and even a possible contribution of the recently discovered urinary microbiome. This review provides a comprehensive overview of our current understanding of kidney stone pathogenesis and identifies new frontiers and remaining gaps in our knowledge of this disease.
... Regarding the urine samples, rare taxa such as Actinomyces, Corynebacterium, Sphingomonas, Anaerococcus, and Bacteroides, and common taxa such as Corynebacterium were found to be enriched in the controls, and common taxa such as Anaerococcus and Corynebacterium were abundant in the patient group. Recently, Al et al. published the results of their study, which focused on the microbiome perturbations found in the stool, urine, stone material, and, additionally, in the saliva of stone formers [91]. Eighty-three stone formers were recruited along with thirty controls, and their biological material was analyzed by 16S rRNA gene sequencing (for urine and saliva samples), and whole shotgun metagenomic sequencing (for stool samples). ...
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... Al et al compared the gut, oral, and urinary microbiota of 30 healthy controls and 83 stone formers and suggested that multisite microbiota alterations may serve as effective indicators of kidney stone development. 22 Mechanistically, oxalate-degrading bacteria, including Oxalobacter formigenes, have been shown to reduce the formation of kidney stones by promoting degradation and modulating the function of the oxalate transporter SLC26A6. 9,23 Short-chain fatty acids, a common group of microbiota-derived metabolites, may also affect kidney stone formation via oxalate transporter modulation and GPR43-dependent immune regulation. ...
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In recent years, there has been an upward trend in the urolithiasis incidence worldwide and an increase in the recurrence of stone formation. Urolithiasis prevalence rates range from 1% to 20%. In some countries, there is an increase in rates up to 37%. Stones are classified into those caused by infections, non infectious causes, and genetic diseases. Alteration in urine microbiome plays a significant role in the infection stone formation. Our objective was to review the current literature on the role of bacteria in the formation of kidney concrements. The gained knowledge could be used to explore new possibilities and improve the understanding of stone formation. We analyzed articles on the composition of the urine microbiome and kidney stones.
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