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. 2023 Dec 28;149(11):860–884. doi: 10.1161/CIRCULATIONAHA.123.065517

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© 2023 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 6. — SGLT2i-induced reduction in uremic toxins translates to humans. A and D, Design of decompensated heart failure (HF) cohort and randomized controlled trial in patients with diabetes. B and C, Decompensated HF: heatmaps of SGLT2i (sodium-glucose cotransporter 2 inhibitor)–induced log2 fold changes for comparisons at discharge (B) and between admission and discharge (C). D, Randomized control trial of patients with diabetes: heatmaps of SGLT2i-induced log2 fold changes for SGLT2i versus placebo (E) and treatment versus baseline (F). SGLT2i treatment reduces uremic toxins originating from aromatic amino acid fermentation.