In adenine-induced chronic kidney disease (CKD) in mice, the level of the uremic toxin indoxyl sulfate increases, leading to increased mucosal expression of the inducible nitric oxide synthase (iNOS) gene.[1] This causes an increase in nitrates in the gut, which promotes the growth of Escherichia coli through nitrate respiration.[1] E. coli produces indole, from which the liver produces indoxyl sulfate, which accelerates the progression of CKD.[1] Faecal microbiota of patients with CKD produce more indole in anaerobic culture than in healthy individuals, but only in the presence of nitrates.[1] The presence of nitrates increases indole production by E. coli and exacerbates kidney damage in CKD mice.[1] Inhibition of iNOS attenuated this harmful pathway in mice.[1] In CKD, stool abundance of Enterobacteriaceae is increased, which is related to these mechanisms.[1]