Alterations of intestinal barrier and microbiota in chronic kidney disease

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.

Chronic Kidney Disease Elicits an Intestinal Inflammation Resulting in Intestinal Dysmotility Associated with the Activation of Inducible Nitric Oxide Synthesis in Rat

“…In CKD progression, many patients are affected by intestinal dysmotility with some main symptoms including abdominal bloating and distension and a mix of nausea and vomiting [5]. Due to declined intestinal motility, enteral feeding or nutrition is often difficult to perform in CKD patients, and therefore, some complications such as intestinal bacterial translocation and malnutrition may be followed by this disorder [1,6,7]. In the previous study, we used the 5/6 kidney resection to induce the rat model of CKD, and then in order to assess this model, the serum creatinine concentrations and blood urea nitrogen and general observations, such as food intake, locomotor, and weight, were assessed at 4 weeks after operation.…”

“…In clinical practice, patients with in- testinal dysmotility could present some main symptoms including abdominal bloating and distension and a mix of nausea and vomiting [5]. Due to a declined intestinal motility, enteral feeding or nutrition is often difficult to perform in CKD patients, and some complications such as intestinal bacterial translocation and malnutrition may be followed by this disorder [1,6,7]. Therefore, CKD patients who are affected by intestinal dysmotility need more medical and social care, thereby increasing the medical costs and impacting the patients' quality of life.…”

Symbiotic Gels: Alternative in Renal Insufficiency

“…It is believed that many factors unrelated and related to dialysis may contribute to the inflammatory condition in CRF, even in the absence of an infectious process, the typical inflammatory state of the disease could be activated and/or enhanced by the passage of molecules and toxins Pro-inflammatory cells from the intestine to the bloodstream a phenomenon called bacterial translocation, where urease-producing microbial families such as Alteromonadacea, Cellulomonadacea, Clostridiacea [22]. microorganisms such as Escherichia Coli metabolize tryptophan producing indole which is subsequently absorbed and is metabolized in the liver to indoxyl sulphate [27], just as when carbohydrate concentrations are low, the amino acids can be subjected to fermentation, and produce Short chain fatty acids and toxins: ammonia, thiols, phenols, and indoles [28] all these phenomena increase uremic toxicity and intestinal barrier dysfunction [29,30].…”

“…Most bacterial species are strictly anaerobic, therefore the bacterial density increases progressively along the intestinal length reaching its maximum in the colon, biotransforming the conjugated bile acids which are molecules involved in the modulation of fat metabolism or glucose [22,23].…”

Berberine Reduces Uremia-Associated Intestinal Mucosal Barrier Damage

“…9) The intestinal tract includes the largest community of bacteria in the body, and the number of microorganisms is much greater than that of the host cells. 10) Under normal conditions, these microorganisms are restricted within the intestinal tract thanks to the integrity of intestinal mucosal barrier.…”