Ann Raes1, Sunny Eloot2, Amina El Amouri3, Evelien Snauwaert1, Aurélie Foulon2, Charlotte Vande Moortel2, Maria Van Dyck4, Koen Van Hoeck5, Nathalie Godefroid6, Griet Glorieux2, Wim Van Biesen2, Johan Vande Walle1. 1. Paediatric Nephrology and Rheumatology Section, Department of Paediatrics, Ghent University Hospital, Corneel Heymanslaan 10, 9000, Ghent, Belgium. 2. Nephrology Section, Department of Internal Medicine and Paediatrics, Ghent University Hospital, Corneel Heymanslaan 10, 9000, Ghent, Belgium. 3. Paediatric Nephrology and Rheumatology Section, Department of Paediatrics, Ghent University Hospital, Corneel Heymanslaan 10, 9000, Ghent, Belgium. amina.elamouri@uzgent.be. 4. Paediatric Nephrology Section, Department of Paediatrics, University Hospitals Leuven (campus Gasthuisberg), Herestraat 49, 3000, Leuven, Belgium. 5. Paediatric Nephrology Section, Department of Paediatrics, Antwerp University Hospital, 2650 Edegem, Antwerp, Wilrijkstraat 10, Belgium. 6. Paediatric Nephrology Section, Department of Paediatrics, Cliniques Universitaires St. Luc, Université Catholique Louvain, Avenue Hippocrate 10, 1200, Brussels, Belgium.
Abstract
BACKGROUND: Chronic kidney disease (CKD) in children is a pro-inflammatory condition leading to a high morbidity and mortality. Accumulation of organic metabolic waste products, coined as uraemic toxins, parallels kidney function decline. Several of these uraemic toxins are protein-bound (PBUT) and gut-derived. Gut dysbiosis is a hallmark of CKD, resulting in a state of increased proteolytic fermentation that might be counteracted by dietary fibre. Data on fibre intake in children with CKD are lacking. We aimed to assess dietary fibre intake in a paediatric CKD cohort and define its relationship with PBUT concentrations. METHODS: In this multi-centre, cross-sectional observational study, 61 non-dialysis CKD patients (9 ± 5 years) were included. Dietary fibre intake was assessed through the use of 24-h recalls or 3-day food records and coupled to total and free levels of 4 PBUTs (indoxyl sulfate (IxS), p-cresyl sulfate (pCS), p-cresyl glucuronide (pCG) and indole acetic acid (IAA). RESULTS: In general, fibre intake was low, especially in advanced CKD: 10 ± 6 g/day/BSA in CKD 4-5 versus 14 ± 7 in CKD 1-3 (p = 0.017). Lower concentrations of both total (p = 0.036) and free (p = 0.036) pCG were observed in the group with highest fibre intake, independent of kidney function. CONCLUSIONS: Fibre intake in paediatric CKD is low and is even worse in advanced CKD stages. Current dietary fibre recommendations for healthy children are not being achieved. Dietary management of CKD is complex in which too restrictive diets carry the risk of nutritional deficiencies. The relation of fibre intake with PBUTs remains unclear and needs further investigation. Graphical abstract.
BACKGROUND: Chronic kidney disease (CKD) in children is a pro-inflammatory condition leading to a high morbidity and mortality. Accumulation of organic metabolic waste products, coined as uraemic toxins, parallels kidney function decline. Several of these uraemic toxins are protein-bound (PBUT) and gut-derived. Gut dysbiosis is a hallmark of CKD, resulting in a state of increased proteolytic fermentation that might be counteracted by dietary fibre. Data on fibre intake in children with CKD are lacking. We aimed to assess dietary fibre intake in a paediatric CKD cohort and define its relationship with PBUT concentrations. METHODS: In this multi-centre, cross-sectional observational study, 61 non-dialysis CKD patients (9 ± 5 years) were included. Dietary fibre intake was assessed through the use of 24-h recalls or 3-day food records and coupled to total and free levels of 4 PBUTs (indoxyl sulfate (IxS), p-cresyl sulfate (pCS), p-cresyl glucuronide (pCG) and indole acetic acid (IAA). RESULTS: In general, fibre intake was low, especially in advanced CKD: 10 ± 6 g/day/BSA in CKD 4-5 versus 14 ± 7 in CKD 1-3 (p = 0.017). Lower concentrations of both total (p = 0.036) and free (p = 0.036) pCG were observed in the group with highest fibre intake, independent of kidney function. CONCLUSIONS: Fibre intake in paediatric CKD is low and is even worse in advanced CKD stages. Current dietary fibre recommendations for healthy children are not being achieved. Dietary management of CKD is complex in which too restrictive diets carry the risk of nutritional deficiencies. The relation of fibre intake with PBUTs remains unclear and needs further investigation. Graphical abstract.
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