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Purpose: In chronic kidney disease (CKD) patients, dysbiosis is associated with inflammation and cardiovascular risk, so many nutritional strategies are being studied to reduce these complications. Resistant starch (RS) can be considered a prebiotic that promotes many benefits, including modulation of gut microbiota which is linked to immune-modulatory effects. The aim of this study was to evaluate the effects of RS supplementation on proinflammatory cytokines in CKD patients on hemodialysis (HD)., Methods: A double-blind, placebo-controlled, randomized trial was conducted with sixteen HD patients (55.3 ± 10.05 years, body mass index (BMI) 25.9 ± 5.42 kg/m 2 , 56% men, time on dialysis 38.9 ± 29.23 months). They were allocated to the RS group (16 g RS/day) or placebo group (manioc flour). The serum concentration of ten cytokines and growth factors was detected through a multiparametric immunoassay based on XMap-labeled magnetic microbeads (Luminex Corp, USA) before and after 4 weeks with RS supplementation., Results: After RS supplementation, there was a reduction of Regulated upon Activation, Normal T-Cell Expressed and Secreted (p < 0.001), platelet-derived growth factor (two B subunits) (p = 0.014) and interferon-inducible protein 10 (IP-10) (p = 0.027). The other parameters did not change significantly., Conclusion: This preliminary result indicates that RS may contribute to a desirable profile of inflammatory markers in CKD patients.

Introduction: Indoxyl sulfate (IS) and p-cresyl sulfate (p-CS) are albumin-bound uremic toxins that are difficult to remove by hemodialysis (HD). Human serum albumin (HSA) carries several compounds, including fatty acids that can bind to site II of HSA and represent competing ligands for uremic toxins. The aim of this study was to investigate the association between fatty acids and uremic toxin plasma levels in patients undergoing HD., Methods: Thirty-three HD patients (51.5% male, 54.9 ± 10.2 years old, 44.63 ± 28.4 months on HD, albumin level of 3.8 ± 0.3 g/dL) were evaluated. The erythrocyte fatty acid content (saturated fatty acid [SFA], monounsaturated fatty acid [MUFA], and polyunsaturated fatty acid [PUFA]) was measured by gas chromatography, and total IS and p-CS plasma levels were measured by reversed-phase high-performance liquid chromatography., Findings: The mean percentages of docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) + DHA and gamma-linolenic (GLA) acid in the erythrocyte membrane were 1.35% ± 0.74%, 1.85% ± 0.79%, and 0.33% ± 0.26%, respectively. The mean levels of IS and p-CS were 19.4 ± 11.9 mg/dL and 101.5 ± 57.2 mg/dL, respectively. There was no significant association between SFA and MUFA and IS and p-CS; however, a negative correlation was found between p-CS and specific PUFAs, and the association between GLA and p-CS levels was retained after adjusting for potential confounding variables (β = -0.49, P = 0.007)., Discussion: Polyunsaturated fatty acids may contribute to the decrease in p-CS uremic toxin plasma levels in patients with chronic kidney disease undergoing HD., (© 2019 International Society for Hemodialysis.)

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.

Under physiologic conditions, the human gut microbiota performs several activities essential to the body health. In contrast, their imbalances exacerbate some actions which can promote a cascade of metabolic abnormalities, and vice versa. Numerous diseases, including chronic kidney disease, are associated with gut microbiota imbalance, and among several strategies to re-establish gut symbiosis, prebiotics seem to represent an effective nonpharmacological approach. Prebiotics fermentation by gut microbiota produce short-chain fatty acids, which improve the gut barrier integrity and function, and modulate the glucose and lipid metabolism as well as the inflammatory response and immune system. Therefore, this literature review intends to discuss the beneficial effects of prebiotics in human health through short-chain fatty acids production, with a particular interest on chronic kidney disease.

Chronic kidney disease (CKD) patients have several metabolic disorders caused by chronic oxidative stress and inflammation. The imbalance of gut microbiota has been identified as a factor that may contribute to the development of these disorders, which can promote cardiovascular disease in CKD patients. Among several strategies to modulate gut microbiota, physical exercise could represent a new nonpharmacological approach. Although exercise can reduce cardiovascular risk in CKD patients through its beneficial effects on oxidative stress and inflammation, there are no available data regarding the relationship between exercise and modulation of gut microbiota in CKD patients. This review is intended to provide a brief overview of the hypothesis regarding gut microbiota modulation through physical exercise, with a particular emphasis on CKD.