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Gut microbiota dynamics and uraemic toxins: one size does not fit all
  1. Marie Joossens1,2,
  2. Karoline Faust1,
  3. Tessa Gryp1,3,4,
  4. Anh Thi Loan Nguyen5,
  5. Jun Wang1,2,6,
  6. Sunny Eloot3,
  7. Eva Schepers3,
  8. Annemieke Dhondt3,
  9. Anneleen Pletinck3,
  10. Sara Vieira-Silva1,2,
  11. Gwen Falony1,2,
  12. Mario Vaneechoutte4,
  13. Raymond Vanholder3,
  14. Wim Van Biesen3,
  15. Geert Roger Bertrand Huys1,2,
  16. Jeroen Raes1,2,
  17. Griet Glorieux3
  1. 1 Laboratory of Molecular Bacteriology– Department of Microbiology and Immunology, KU Leuven, Leuven, Belgium
  2. 2 Center for Microbiology, VIB, Leuven, Belgium
  3. 3 Department of Internal Medicine and Pediatrics, Nephrology Section, Ghent University Hospital, Ghent, Belgium
  4. 4 Department of Clinical Chemistry, Microbiology and Immunology, Laboratory Bacteriology Research, Ghent University, Ghent, Belgium
  5. 5 Address of current employer: Clinical Research SGS, Life Science Services, Mechelen, Belgium
  6. 6 Current address: CAS Key Laboratory for Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China
  1. Correspondence to Professor Griet Glorieux, Department of Internal Medicine, Nephrology Division, Ghent University Hospital, Ghent 9000, Belgium; griet.glorieux{at}

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In the recent paper by Chu and colleagues,1 the potential role of microbiota-related metabolites in the progression of non-alcoholic fatty liver disease is discussed. This topic has been studied in the context of chronic kidney disease (CKD), characterised by changes in gut microbiota composition,2 accumulation of microbiota-derived metabolites,3 interruption of intestinal barrier function and chronic inflammation.4 In line with this, we focused, in a cohort of 17 patients with end-stage kidney disease (ESKD), on the role of gut microbiota in the generation of precursors of specific uraemic toxins which are associated with negative outcomes in these patients.5 By collecting multiple samples over time, assessment of variability within and between patients in relation to disease progress and clinical variables was possible. Faecal and serum samples were collected at eight time-points over a 4-month period (online supplementary table 1). Uraemic metabolites and microbial profiling were determined by HPLC and 16S rRNA amplicon sequencing, respectively (see Supplementary data). Variation in microbial profiles of patients with ESKD was compared with that of 1106 subjects from a population-based cohort, the Flemish Gut Flora Project (FGFP),6 which have a similar genetic and environmental background as well as to a subset of age-matched controls of comparable health status (n=32).

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In this longitudinal study, within-patient analyses showed that variations in peripheral levels of p-cresyl conjugates (the composite of p-cresyl sulfate (pCS)/glucuronide (pCG); pC), indoxyl sulfate (IxS), indole acetic acid and …

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