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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Cardiovascular-Kidney-Metabolic (CKM) syndrome, defined by converging metabolic, kidney, and cardiovascular disorders, represents a substantial global health burden. Accumulating evidence has established a link between the gut microbiota and CKM syndrome. However, its specific role in disease progression has not been fully elucidated.
To investigate the microbial drivers of CKM syndrome progression, we conducted metagenomic and untargeted metabolomic analyses on fecal samples from 38 non-advanced (stages 0-2) and 30 advanced (stages 3-4) patients.
Beta diversity analysis revealed a significant difference in overall microbial composition between the advanced and non-advanced CKM groups (Figure 1A, P = 0.022). LEfSe analysis showed enrichment of the Enterobacteriaceaefamily, Flavonifractor plautii, and Ruthenibacterium lactatiformans in the advanced CKM group, whereas eight species-including Bacteroides uniformis, Gemmiger formicilis and Alistipes putredinis, were enriched in the non-advanced CKM group (Figure 1B, P<0.05). KEGG analysis of metagenomic and metabolomic data consistently identified alterations in two vitamin metabolic pathways (vitamin B6; nicotinate and nicotinamide) and three amino acid metabolic pathways (cysteine and methionine; taurine and hypotaurine; tryptophan) in CKM syndrome (Figure 1C, D, P < 0.05). Metabolites from amino acid pathways, L-cysteine and 3‑hydroxyanthranilic acid, were increased and positively correlated with the abundance of F. plautii and R. lactatiformans in the advanced CKM group. In contrast, vitamin-related metabolites—such as nicotinic acid, pyridoxamine and pyridoxal 5‑phosphate—were depleted and showed positive correlations with species including G. formicilis and A. putredinis (Figure 1E, P<0.05). A random forest model combining F. plautii, L-cystine and 3‑hydroxyanthranilic acid achieved an AUC of 0.861 (0.768–0.953) for distinguishing advanced from non-advanced CKM after 10-fold cross validation (Figure 1F).
Collectively our findings suggest that gut microbiota alterations disrupt key metabolic pathways with associated metabolites —including vitamins B6, nicotinate and nicotinamide, and amino acid metabolisms of cysteine and methionine, taurine and hypotaurine, and tryptophan—whose dysregulation may accelerate CKM syndrome progression. A combination of F. plautii, L-cystine and 3‑hydroxyanthranilic acid may serve as a non-invasive detection on CKM syndrome.
