One of the greatest challenges in diabetic kidney disease (DKD) is fibrosis—the gradual scarring of kidney tissue that continues even when patients maintain strong control of blood sugar and blood pressure. A new study has revealed an unexpected factor that may help explain this progression: a molecule produced by gut bacteria.
What the Study Found
Researchers at the University of Illinois Urbana-Champaign and Mie University in Japan have identified a bacterial peptide called corisin, produced by certain gut microbes. Corisin travels from the gut into the bloodstream, often binding to albumin, a major blood protein. Once detached, it can infiltrate kidney tissue. There, it accelerates aging in kidney cells, increases inflammation, promotes cell death, and contributes to fibrosis.
Patients with diabetic kidney fibrosis were found to have significantly higher levels of corisin in their blood compared to healthy individuals. In animal models, corisin sped up kidney damage, but when treated with an antibody that neutralized corisin, the progression of fibrosis slowed, with less scarring and fewer signs of cellular aging.
Why This Matters
Despite the use of proven therapies—such as glucose control, blood pressure management, and reduction of protein in the urine—fibrosis often continues in patients with DKD. Corisin may account for part of this residual risk. If further validated, corisin could become both a biomarker for disease progression and a therapeutic target. Neutralizing this molecule may offer a new line of treatment alongside current standards of care, while also emphasizing the growing importance of the gut–kidney connection in chronic disease.
What Remains Unknown
Although promising, these findings are still in the early stages. Human studies are needed to confirm whether targeting corisin is safe and effective. It is also unclear whether individual differences in gut bacteria or in how the body processes albumin influence corisin levels and kidney damage. Importantly, the research suggests neutralizing corisin can slow progression, but it does not yet show the ability to reverse existing scarring.
Clinical Implications
For patients, this research should not replace existing therapies. Careful management of blood sugar, blood pressure, and medications, combined with healthy lifestyle practices, remains the foundation of kidney health. Still, the discovery of corisin represents new hope that more precise treatments could one day reduce the risk of kidney scarring before it becomes irreversible.
For healthcare providers, corisin may eventually become a useful biomarker for identifying high-risk patients and guiding treatment decisions. It also highlights the growing relevance of the microbiome in nephrology, where gut-derived molecules can directly influence kidney outcomes.
Conclusion
The identification of corisin as a potential driver of diabetic kidney fibrosis opens new possibilities for diagnosis and treatment. While more research is needed, this discovery could shape the future of care for patients with diabetic kidney disease.
For individuals living with kidney disease or at risk of developing it, now is the time to stay proactive. To learn more about kidney health and personalized care options, schedule an appointment with Northlake Nephrology Institute today.
Reference: Yasuma, T., Fujimoto, H., D’Alessandro‐Gabazza, C. N., et al. Microbiota‐derived corisin accelerates kidney fibrosis by promoting cellular aging. Nature Communications. 2025. DOI: 10.1038/s41467-025-61847-2 (ScienceDaily summary)
