Dysbiosis may favor the occurrence of inflammation and oxidative stress in chronic kidney disease (CKD). It has been suggested that the intake of pre/probiotics may control the progression of chronic kidney disease. Thus, the objective of this study was to systematically review the literature on the effects of pre/probiotic intake on the intestinal microbiota, control of nitrogen products, oxidative stress, and inflammation in CKD patients.The literature search was conducted on MEDLINE, LILACS, Cochrane Library of Clinical Trials, and Science Direct. After careful evaluation by the reviewers, ten potentially relevant articles were selected for this study. Based on previous studies, intake of prebiotics appears to have the following effects: increased bifidobacteria and lactobacillus counts; reduced formation of uremic toxin, p-cresol, and its serum concentrations; improved lipid profiles; reduced systemic inflammatory state and concentrations of oxidative stress markers. Similarly, consumption of probiotics can reduce blood urea and serum phosphate concentrations. Furthermore, an increase in fecal volume and intestinal Bifidobacteriumand a reduction in p-cresol serum and blood urea concentrations were observed in response to symbiotic intake. These results suggest that consumption of pre/probiotics may modulate the intestinal microbiota, and promote the growth and metabolism of anaerobic bacteria by decreasing the production of uremic solutes, further causing oxidative stress and systemic inflammation in CKD patients.

Cardiovascular disease (CVD) is one of the leading causes of mortality in hemodialysis (HD) subjects. In addition to the traditional risk factors that are common in these individuals, genetic factors are also involved, with emphasis on single nucleotide polymorphs (SNPs). In this context, the present study aims to systematically review the studies that investigated the polymorphisms associated with cardiovascular risk in this population. In general, the SNPs present in HD individuals are those of genes related to inflammation, oxidative stress and vascular calcification, also able of interfering in the cardiovascular risk of this population. In addition, polymorphisms in genes related to recognized risk factors for CVD, such as dyslipidemia, arterial hypertension and left ventricular hypertrophy, also influence cardiovascular morbidity and mortality.

mGSA and GOA were more sensitive with respect to identifying individuals at nutritional risk compared to the isolated anthropometric indicators, thus indicating their utility in diagnostic malnutrition. However, individuals at high nutritional risk also presented cardiometabolic risk, as diagnosed mainly by central fat indicators, suggesting the application of both malnutrition and cardiometabolic risk markers in HD patients.

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Those individuals with a high concentration of NO (> 4.32 μmol/L) had lower values for SGAm score (p = 0.012) and higher iron values (p = 0.050), Fe saturation (p = 0.037) and triacylglycerol (p = 0.003). The same subjects still had lower consumption of copper (p = 0.026), manganese (p = 0.035), vitamin E (p = 0.050), ω3 (p = 0.021) and ω6 (p = 0.020). In a multiple regression model, concentrations of ferritin, triacylglycerol, IL6 and SOD contributed to a 54.8% increase in NO concentrations, whereas triacylglycerol and SOD concentrations were independent factors for NO variation (p < 0.001). CONCLUSIONS: The clinical and nutritional status as well as intake of nutrients with antioxidant properties (Cu, Zn, Mn, vitamin C and ω3) appears to modulate the variation of NO in this population.