This review summarizes the dysbiosis of gut microbiota in kidney disease and elucidates the underlying molecular mechanisms of microbial dysbiosis through a broad spectrum of signaling pathways, such as TGF-β/Smad, IκB/NF-κB, Keap1/Nrf2, phosphatidylinositol-3 kinase (PI3K), and mitogen-activated protein kinases (MAPK), as well as key mediators, such as AHR, NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, and G protein-coupled receptor 43 (GPR43), via alteration of diverse metabolites. This evidence concerns the gene FFAR2 and kidney disorder.