Researchers have discovered that a small molecule produced by gut bacteria travels to the kidneys and triggers a cascade of inflammation, scarring, and fibrosis, causing one of the serious complications of diabetes and the leading cause of kidney failure.

The study was conducted by researchers from the University of Illinois Urbana-Champaign in the United States and the University of Mie in Japan. The results were published in the journal Nature Communications on August 25, 2025, and reported by EurekAlert.

Scientists found high levels of corisin—a small peptide produced by Staphylococcus aureus bacteria in the gut—in the blood of diabetic kidney fibrosis patients. They used computer simulations and experiments on tissues and mice to track how corisin affects the kidneys, how it reaches them from the gut, and a potential way to counter it using antibody therapy.

Isaac Kang, Professor of Animal Sciences at the University of Illinois and lead author of the study, said: “Our previous studies showed that corisin can damage cells and increase tissue scarring and fibrosis in other organs, so we suspected it might be a hidden factor in kidney fibrosis.”

He added: “Our new findings indicate that corisin is indeed a hidden factor behind progressive kidney damage in diabetic patients, and blocking it could offer a new way to protect kidney health.”

Many chronic diabetic patients eventually develop kidney fibrosis, and once the condition worsens, treatment options become limited.

Dr. Taro Yasuma from the University of Mie, a physician and co-author, said: “Diabetic kidney fibrosis is a leading cause of kidney failure worldwide, but the main causative factors remain unclear, and no treatment can stop this process.”

Current treatments mainly focus on controlling blood sugar and blood pressure, but no cure exists to halt or reverse scarring or fibrosis, Yasuma added.

The researchers began by examining blood and urine from diabetic patients and found that corisin levels were much higher than in healthy controls, and the amount of corisin in the blood correlated with the extent of kidney damage.

Observing similar results in mice with kidney fibrosis, the team tracked corisin’s effects in their kidneys. They found corisin accelerates kidney cell aging, triggering a series of reactions starting with inflammation, then cell death, followed by scar tissue accumulation, ultimately leading to kidney function loss and worsening fibrosis.

How does corisin travel from the gut to the kidneys? Kang and Gabazza’s groups collaborated with Diwakar Shukla, Professor of Chemical and Molecular Bioengineering at the University of Illinois, to produce computer simulations and lab experiments tracing corisin’s journey from the gut to the bloodstream.

They found corisin binds to albumin, one of the most common proteins in the blood, and travels through the bloodstream. Upon reaching the kidneys, corisin detaches from albumin to attack the delicate structures that filter blood and urine.

To confirm corisin’s key role in kidney damage, researchers administered anti-corisin antibodies to mice and observed a significant reduction in the rate of kidney damage.

Gabazza, also an assistant professor of animal sciences at the University of Illinois, said: “Treating mice with an antibody that neutralizes corisin slowed kidney cell aging and significantly reduced kidney scarring.”

He added: “Although no antibody is currently approved for human use, our results suggest the potential for developing it as a new treatment.”