No abstract

Gut microbiota imbalance is common in patients with chronic kidney disease (CKD) and associates with factors such as increased circulating levels of gut-derived uremic toxins, inflammation, and oxidative stress, which are linked to cardiovascular disease and increased morbimortality. Different nutritional strategies have been proposed to modulate gut microbiota, and could potentially be used to reduce dysbiosis in CKD. Nutrients like proteins, fibers, probiotics, and synbiotics are important determinants of the composition of gut microbiota and specific bioactive compounds such as polyphenols present in nuts, berries. and fruits, and curcumin, may also play a key role in this regard. However, so far, there are few studies on dietary components influencing the gut microbiota in CKD, and it is therefore not possible to conclude which nutrients should be prioritized in the diet of patients with CKD. In this review, we discuss some nutrients, diet patterns and bioactive compounds that may be involved in the modulation of gut microbiota in CKD and provide the background and rationale for studies exploring whether nutritional interventions with these dietary components could be used to alleviate the gut dysbiosis in patients with CKD.

Prebiotic-resistant starch supplementation may be a good strategy to reduce inflammation, oxidative stress and uremic toxins in CKD patients.

stress and premature ageing are common features of the uremic phenotype.• The foodome -defined as the pool of all compounds present in a food sample and/or in a biological system interacting with the investigated food -can be implicated in the modulation of CKD complications.• Imbalance in the relative diversity of the gut microbiota has been studied extensively in CKD due its links with inflammation and cardiovascular risk. In this direction, researchers are evaluating the effects of pre-, pro-and synbiotics and many others food components like polyphenol-rich foods, sugar, proteins, etc. on both the modulation of the diversity of the gut microbiota and reduction in the levels of uremic toxins .• The use of bioactive compounds, found in curcumin, broccoli sprouts, berries, propolis, etc. may be valid nutritional therapeutic agents to modulate the expression of pro-inflammatory transcription factors, such as Nrf2, NF-kB and the inflammasome.• Senotherapeutic dietary compounds may mitigate the effects of a dysregulated ageing process in CKD and associated complications. including disturbed mitochondrial metabolism.Onion and garlic -may decrease NLRP3 activation Spinach -rich in betaine Green leafy vegetables -rich in folate Cruciferous vegetables, -rich in sulforaphane -may decrease NLRP3 activation, Nrf2 activators Some vegetables, such as spinach, broccoli, potatoes, cucumbers, green leafy -rich in potassium.

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor involved in the expression of xenobiotic-metabolizing enzymes, inflammatory cytokines and adhesion molecules. Uremic toxins such as indoxyl sulfate and indole acetic acid are derived from tryptophan fermentation by gut microbiota; they accumulate in patients with chronic kidney disease (CKD) on haemodialysis and have recently emerged as potent ligands of AhR. Therefore, AhR can serve as a mediator in inflammation and cardiovascular diseases in these patients. This review discusses current data that support a link between AhR activation and uremic toxins from gut microbiota in CKD.

No abstract

Components present in the diet, L-carnitine, choline, and betaine are metabolized by gut microbiota to produce metabolites such as trimethylamine-N-oxide (TMAO) that appear to promote cardiovascular disease in chronic kidney disease (CKD) patients. The objective of this pilot study was to evaluate the effects of probiotic supplementation for 3 months on plasma TMAO levels in CKD patients on hemodialysis (HD). A randomized, double-blind trial was performed in 21 patients [54.8 ± 10.4 years, nine men, BMI 26.1 ± 4.8 kg/m, dialysis vintage 68.5 (34.2-120.7) months]. Ten patients were randomly allocated to the placebo group and 11 to the probiotic group [three capsules, totaling 9 × 10 colony-forming units per day of Streptococcus thermophilus (KB19), Lactobacillus acidophilus (KB27), and Bifidobacteria longum (KB31). Plasma TMAO, choline, and betaine levels were measured by LC-MS/MS at baseline and after 3 months. While TMAO did not change after probiotic supplementation, there was a significant increase in betaine plasma levels. In contrast, the placebo group showed a significant decrease in plasma choline levels. Short-term probiotic supplementation does not appear to influence plasma TMAO levels in HD patients. Long-term studies are needed to determine whether probiotics may affect TMAO production in CKD patients.

Although CKD patients did not present altered gut microbial profile, the sequencing of bands suggested a different microbiota between groups. The result suggests a possible relationship between gut microbiota and cardiovascular risk in CKD patients.