Gut Microbiota Dysbiosis Is a Key Driver of Inflammaging in Chronic Kidney Disease

The role of gut microbiota and intestinal dysbiosis in promoting inflammaging in chronic kidney disease (CKD) has been the focus of intense research over the last years. Some alterations at the phyla level, such as abundance of Proteobacteria and reduction in Firmicutes/Bacteroidites (F/B) ratio and saccarolytic populations, have been consistently reported in CKD. Other mechanisms include microbial translocation through a "leaky gut" and subsequent molecular mimicry, immune dysregulation (unbalance between T reg and Th17 subsets), and epigenetic interactions. Alterations of metabolic pathways and of bacterial metabolites, such as butyrate and other short chain fatty acids (SCFA), also appear to play a key role in modulating progression of CKD. On the other hand, microbiota-based therapy appears promising and includes diet, prebiotics, probiotics, synbiotics, postbiotics and fecal microbiota transplantation (FMT). Modulation of microbiota could correct critical alterations, such as F/B ratio and T reg/Th17 unbalance, blunting inflammaging and potentially reducing progression of CKD and cardiovascular disease. Despite current limitations, gut microbiota is emerging as a powerful environmental factor which could be harnessed to interfere with key mechanisms leading to inflammaging in CKD.