Uncovered mechanisms involved in this dialogue between the intestine and kidneys account for enhancing kidney inflammation, such as proteins and metabolites produced in the intestine that may cause kidney inflammation (e.g., immunoglobulin A (IgA) deposition, p-cresyl sulfate, and indoxyl sulfate) (Han et al., 2016; Lin et al., 2019; Cheng et al., 2020) whereas others prevent kidney lesions (e.g., short-chain fatty acids (SCFAs)) (Andrade-Oliveira et al., 2015) (Figure 1). This evidence concerns the gene CD79A and nephritis.