Researchers have identified high levels of a molecule called corisin in the blood of patients with diabetic kidney fibrosis, linking it to the progression of this serious complication.

Corisin, produced by gut bacteria such as Staphylococcus species, can travel from the intestine to the kidneys by attaching to albumin in the bloodstream, where it detaches to damage kidney tissues.

Corisin interacts with albumin, which helps it travel through the blood and enhances its stability and damaging activity, ultimately attacking the kidney's filtering structures.

This molecule accelerates aging, inflammation, cell death, and scarring in kidneys, contributing to the progression of diabetic chronic kidney disease (CKD).

The study, published in Nature Communications, combines microbiology, immunology, and clinical sciences, and suggests that targeting corisin could lead to new molecular and microbiome-based therapies for CKD.

Laboratory experiments and molecular simulations indicate that corisin reaches the kidneys by attaching to albumin, which acts as a carrier, facilitating its transport and pathogenic effects.

Future research will focus on testing anticorisin therapies in larger animal models like pigs to evaluate safety and effectiveness, aiming to translate these findings into human treatments.

These upcoming studies will validate corisin's role in kidney fibrosis and develop therapeutic strategies suitable for clinical application in humans.

Corisin's interaction with albumin not only stabilizes it but also amplifies its proapoptotic and pathogenic effects in diabetic nephropathy.

Staphylococcus species are identified as the primary source of corisin in diabetic patients with CKD, with peptides matching those from various bacteria found in urine samples.

Corisin bypasses immune detection by attaching to albumin, then detaching in the kidneys to initiate damaging inflammatory pathways.

This interdisciplinary research opens new avenues for developing microbiome-based therapies to combat chronic kidney disease.