Moreover, an increasing amount of studies have also established a relevant role of gut-derived tryptophan metabolites (namely IS, 3-IS and indole-3 acetic acid (IAA)), in renal fibrosis through the activation of aryl hydrocarbon receptor signaling pathways, specifically, through activation of aryl hydrocarbon receptor/p38 mitogen-activated protein kinase/NF-κB pathways that regulate cell proliferation, differentiation and immune function and induce cardiovascular disease in ESRD patients [102]. This evidence concerns the gene AHR and cardiovascular disorder.