Table 3:

Evidence for role of microbiota in chronic kidney disease

Tang et al 2015, Warrior et al. 2015; Zhu et al. 2016, Tand et al. 2013	Gut microbial metabolite trimethylamine-N-oxide (TMAO) directly contributes to progressive renal fibrosis and dysfunction in animal models; increases mortality risk in CKD; enhances platelet hyperreactivity and thrombosis risk; regulates lipid metabolism and inflammation; TMAO may be linked to specific dietary nutrients and gut microbes.
Wang et al. 2012	Experimental uremia in rats increases bacterial translocation from gut, which is associated with higher serum IL-6 and C-reactive protein levels. (Wang 2012)
McIntyre et al. 2011	Progressive levels of circulating bacterial endotoxin and LPS with CKD are highest in patients on dialysis. LPS levels are an independent predictor of mortality.
Anders et al. 2007	Bacterial products activate pattern-recognition receptors on various immune cells inside and outside the kidney.
Kiechl et al. 2002	Increased LPS/TLR-4 signaling may promote accelerated atherogenesis in CKD.
Ranganathan et al. 2006	Oral intake of nonpathogenic Sprosarina pasteurii improved renal function and survival of uremic rats.
Niwa et al. 2011	Oral neutralization of indoxyl sulfate (a bacteria-derived uremic toxin) delays progression of CKD and cardiovascular disease in uremic rats.