Introduction Chronic kidney disease (CKD), a debilitating condition, results in systemic inflammation and oxidative stress. This leads to progression of kidney disease and the associated complications including cardiovascular disease, cachexia, and anemia. The gastrointestinal tract is recognized as a major source of this systemic inflammation and oxidative stress as the intestinal microbiome is markedly altered in CKD (Table 1). Altered microbiome results in increased production of bacteria-derived uremic toxins such as indoxyl sulphate, p-cresyl sulphate, and trimethylamine- N-oxide (TMAO). Role for gut-derived uremic toxins has been established in varied studies in promoting multiorgan dysfunction (Figure 1) via inflammatory, oxidative stress, and apoptosis pathways. Indoxyl sulfate and p-cresyl sulfate are well characterized uremic toxins that induce inflammation and leukocyte activation and have been associated with increased systemic inflammation and mortality in CKD patients. TMAO is a toxin generated by conversion of choline to trimethylamine by the gut microbial flora. Elevated levels of TMAO have been linked to increased 5-years mortality risk in CKD subjects after multivariate adjustment. Levels of circulating endotoxin, increase with severity of CKD stage and are most elevated in end-stage renal disease (ESRD) patients on maintenance dialysis.