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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Although low-protein diet (LPD) slows CKD progression, its metabolic mechanisms remain unclear. Given adherence challenges and PEW risk, this study examined whether LPD improves metabolic health through uremic toxin (UT) reduction, improved glucose metabolism, and microbiota changes, focusing on fibroblast growth factor 21 (FGF21), a liver hormone that responds to protein restriction by promoting food intake and increasing energy expenditure in both CKD mice and humans. It also tested whether Lactiplantibacillus plantarum (LpWJL)—identified for growth promotion under nutrient restriction—could alleviate LPD-induced metabolic stress and PEW by modulating amino acid levels and FGF21 in CKD mice.
16 non-diabetic CKD patients were randomized to a 3-month LPD with ketoanalogues (0.4 g/kg/day, n=7) or a normal-protein diet (ND; 0.8 g/kg/day, n=9) (NCT03959228). Body composition, glucose tolerance, UT, and gut microbiota (16S rRNA sequencing) were assessed at baseline and 3 months. In mice, 5 groups were studied: sham-operated (ND, 21% protein), 5/6 nephrectomized (ND), and 5/6 nephrectomized fed LPD (5% protein) with or without LpWJL (2 × 108 CFU, 5 days/week) for 6 weeks. Plasma metabolomics were analyzed by LC-MS/MS (Biocrates).
Energy intake was similar across groups. LPD reduced body weight in both humans (−1.4 kg; p < 0.05) and mice (−4 g; p < 0.001), improved glucose tolerance, and lowered circulating UT. Indoxyl sulfate (IS) and trimethylamine N-oxide positively correlated with glucose intolerance. LPD modified gut microbiota functions, especially pathways linked to aromatic amino acid biosynthesis. LpWJL + LPD preserved body weight, body length, and fat mass, while sustaining glucose tolerance. In plasma, LpWJL increased circulating amino acid levels and decreased UTs, notably IS. LPD induced a marked increase in plasma FGF21 levels in both mice and humans; FGF21 levels were positively associated with glucose tolerance but inversely correlated with body mass. This FGF21 response was attenuated by LpWJL supplementation in mice.
These findings identify UTs and FGF21 as central mediators of the metabolic response to dietary protein restriction in CKD, and support microbiota-targeted strategies—such as LpWJL supplementation,as promising approaches to enhance the metabolic tolerance and clinical efficacy of LPD.
