Alterations of intestinal barrier and microbiota in chronic kidney disease

Nephrol Dial Transplant. 2015 Jun;30(6):924-33. doi: 10.1093/ndt/gfu287. Epub 2014 Sep 4.

Abstract

Recent studies have highlighted the close relationship between the kidney and the gastrointestinal (GI) tract--frequently referred to as the kidney--gut axis--in patients with chronic kidney disease (CKD). In this regard, two important pathophysiological concepts have evolved: (i) production and accumulation of toxic end-products derived from increased bacterial fermentation of protein and other nitrogen-containing substances in the GI tract, (ii) translocation of endotoxins and live bacteria from gut lumen into the bloodstream, due to damage of the intestinal epithelial barrier and quantitative/qualitative alterations of the intestinal microbiota associated with the uraemic milieu. In both cases, these gut-centred alterations may have relevant systemic consequences in CKD patients, since they are able to trigger chronic inflammation, increase cardiovascular risk and worsen uraemic toxicity. The present review is thus focused on the kidney-gut axis in CKD, with special attention to the alterations of the intestinal barrier and the local microbiota (i.e. the collection of microorganisms living in a symbiotic coexistence with their host in the intestinal lumen) and their relationships to inflammation and uraemic toxicity in CKD. Moreover, we will summarize the most important clinical data suggesting the potential for nutritional modulation of gut-related inflammation and intestinal production of noxious by-products contributing to uraemic toxicity in CKD patients.

Keywords: chronic kidney disease; endotoxin; inflammation; intestinal microbiota; uraemic toxicity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cardiovascular Diseases / etiology*
  • Gastrointestinal Tract / microbiology*
  • Humans
  • Intestines / microbiology
  • Intestines / pathology*
  • Microbiota*
  • Renal Insufficiency, Chronic / complications*
  • Renal Insufficiency, Chronic / microbiology
  • Renal Insufficiency, Chronic / pathology
  • Risk Factors