Gut microbiota dysbiosis in diabetic kidney disease is associated with a reduced abundance of short-chain fatty acid-producing bacteria (e.g., Faecalibacterium, Roseburia) and an increased abundance of proteolytic bacteria that generate uremic toxins such as indoxyl sulfate and p-cresyl sulfate, which contribute to systemic inflammation and renal fibrosis via oxidative stress and activation of the aryl hydrocarbon receptor pathway.

In diabetic kidney disease, the gut bacteria that make beneficial short-chain fatty acids decrease, while bacteria that break down protein increase. These protein-digesting bacteria produce toxic chemicals that enter the blood, reach the kidneys, and activate a receptor called AhR. This receptor turns on harmful pathways that damage kidney cells, cause oxidative stress, and trigger scarring. At the same time, the loss of short-chain fatty acids weakens the gut barrier, allowing more toxins and bacterial fragments to leak into the bloodstream, worsening kidney damage.