A new discovery has the potential to slow the progression of kidney disease in people with diabetes and prevent renal failure by supporting the normal function of the mitochondria within the kidney.

The five-year study initially discovered that a key immune system pathway – which usually protects the body from infection – was hyperactivated and caused inflammation in people with diabetic kidney disease.

The team led by Associate Professor Melinda Coughlan from the Department of Diabetes then discovered this pathway could be disrupted with a drug (developed by Associate Professor Trent Woodruff, from the School of Biomedical Sciences at the University of Queensland) which could help to support the normal function of the mitochondria within the kidney – known as the “batteries of the cell” – which don’t work properly in people with diabetes.

According to the World Health Organisation, more than 420 million people have diabetes, with 1.5 million of them dying from a diabetes-related disease each year. It’s also the leading cause of renal failure with an estimated 1 in 4 diabetic adults having had kidney disease, which can cause other health problems later in life.

Therapy could prevent renal failure in people with diabetic kidney disease

Associate Professor Coughlan said their discovery could potentially lead to a therapy to delay or prevent renal failure in people with diabetic kidney disease.

“We’re saying this is a new link between the immune system and the mitochondria, which could also help patients with diabetic kidney disease by boosting mitochondrial health – so it could protect the kidney in patients with diabetes,” Associate Professor Coughlan said.

“Findings like this will become important for managing the health of people with diabetes. The economic burden of diabetes is huge, and this could potentially help reduce that.”

Associate Professor Coughlan, whose work includes investigating dietary factors leading to the onset of diabetes and its complications, said they would now look at developing medicines that target this pathway for future use in the clinic.