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From kidney to liver: Are sodium–glucose cotransporter-2 inhibitors emerging as metabolic disease modifiers?
Sydney Mpisa, Jonathan Soldera, MSc Acute Medicine and Gastroenterology, University of South Wales in association with Learna Ltd, University of South Wales, Cardiff CF37 1DL, United Kingdom
Jonathan Soldera, Department of Gastroenterology, Logan Hospital, Brisbane 4101, Queen
Author contributions: Soldera J, Mpisa S participated in the concept and design research, drafted the manuscript and contributed to data acquisition, analysis and interpretation; Soldera J contributed to study supervision; all authors contributed to critical revision of the manuscript for important intellectual content.
AI contribution statement: Limited use of artificial intelligence tools was made to assist in language polishing and summarization tasks. However, no part of the manuscript was entirely generated by artificial intelligence; instead, it underwent extensive manual input by the author, rigorous review, and revision. Artificial intelligence tools did not participate in research design, data collection, statistical analysis, or result interpretation. All scientific content, conclusions, and final wording were determined by the author. No artificial intelligence-generated charts, images, or graphic elements were used in the manuscript.
Conflict-of-interest statement: The authors declare to have no conflict of interest.
PRISMA 2009 Checklist statement: The authors have read the PRISMA 2009 Checklist, and the manuscript was prepared and revised according to the PRISMA 2009 Checklist.
Corresponding author: Jonathan Soldera, MSc Acute Medicine and Gastroenterology, Uni
Received: March 30, 2026
Revised: April 28, 2026
Accepted: May 21, 2026
Published online: September 25, 2026
Processing time: 137 Days and 2.3 Hours
Revised: April 28, 2026
Accepted: May 21, 2026
Published online: September 25, 2026
Processing time: 137 Days and 2.3 Hours
Core Tip
Core Tip: Sodium-glucose cotransporter-2 inhibitors extend beyond glycaemic control and may modify key pathways of metabolic disease. Evidence from diabetic kidney disease and metabolic dysfunction-associated steatotic liver disease suggests these agents attenuate inflammation and fibrosis, with a potential association with reduced hepatocellular carcinoma incidence. This supports a shift toward integrated, cross-organ metabolic disease modification.