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. Author manuscript; available in PMC: 2018 May 31.
Published in final edited form as: Expert Rev Clin Pharmacol. 2017 Sep 20;11(1):71–82. doi: 10.1080/17512433.2018.1378095

Figure 1.

Figure 1

The intestinal microbiota produces several microbial toxins that extensively accumulate in kidney disease likely due to increased toxin producing bacterial species and decreased renal clearance. Microbiota-derived uremic toxins such as p-cresol sulfate, indoxyl sulfate, indole-3-acetic acid, CMPF, kynurenic acid, and hippuric acid perpetrate interactions with phase I/II metabolic enzymes and drug transporters. These interactions occur in the liver and kidneys at the translational and post-translational levels. Patients with kidney disease are at increased risk for adverse drug events, and these accumulated microbiota-derived uremic toxins likely contribute to altered drug disposition.