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Butyrate production in patients with end-stage renal disease

Authors Terpstra ML, Sinnige MJ, Hugenholtz F, Peters-Sengers H, Remmerswaal EBM, Geerlings SE, Bemelman FJ

Received 3 January 2019

Accepted for publication 28 February 2019

Published 6 May 2019 Volume 2019:12 Pages 87—101

DOI https://doi.org/10.2147/IJNRD.S200297

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Professor Pravin Singhal


Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman1

1Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands

Background: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.
Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.
Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.
Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.

Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation

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