Mater Research’s Professor Josephine Forbes has recently published a review in Nature Reviews Nephrology investigating mitochondrial dysfunction in diabetic kidney disease.
Globally, diabetes is the leading cause of chronic kidney disease and end-stage renal disease, which are major risk factors for cardiovascular disease and death. Despite this burden, the factors that trigger the development and progression of diabetic kidney disease are not fully understood.
An estimated 1.2 million (6%) of Australian adults aged 18 years and over had diabetes in 2014–15. This includes people with both type 1 or type 2 diabetes, but excludes gestational diabetes.
Diabetes can damage the kidney filters, leading to diabetic kidney disease. Around half of people who begin dialysis or require a transplant have end stage kidney disease caused by diabetes. The longer a person has diabetes, the more likely they are to develop kidney damage. Kidney damage is also an important risk factor for heart attacks, stroke and premature death in individuals with diabetes.
Mitochondrial dysfunction is associated with kidney disease in non-diabetic contexts, and increasing evidence suggests that mitochondria dysfunction is a key indicator of diabetic kidney disease.
Professor Forbes explains her research in the midst of a global diabetes pandemic, with a third of patients with diabetes going on to develop cardiovascular and kidney disease.
“We’ve recently discovered that kidney disease starts much earlier than previously appreciated,” Professor Forbes said.
“We’re particularly interested in the function of ‘cell power stations’ which are called mitochondria. We know that young people aged 15-25 have evidence of dysfunction in these cell power stations but we may be able to detect this even earlier to start treatment to prevent kidney disease.”
The kidneys are highly metabolic organs rich in mitochondria. They contain vast numbers of mitochondria to synthesise fuel (adenosine triphosphate (ATP)), for their normal function. In diabetes, the delivery of metabolic products such as fatty acids and oxygen, which are essential for ATP production in mitochondria, are altered. Diabetes also changes the fuel sources chosen to meet ATP production, resulting in increased oxygen consumption, which contributes to a lack of oxygen (hypoxia) in the kidneys.
“As a result, in our paper we suggest that the diabetic environment and inherited factors that underlie abnormalities in mitochondrial function synergistically drive the development and progression of diabetic kidney disease,” Professor Forbes said.
This research played a role in Professor Forbes winning the 2018 Strategic Grant for Outstanding Women. The Mater Research Strategic Grants for Outstanding Women are proudly funded through Mater Foundation’s generous donors and supporters.
Mater Research is committed to supporting women in research and was awarded the Employer of Choice – Small Business at the 2017 Women in Technology Awards.
https://www.ncbi.nlm.nih.gov/pubmed/29456246