Understanding the relationship between mitochondrial damage, immune activation and diabetic kidney disease risk in children and adolescents with newly diagnosed type 1 diabetes.
Rationale: Individuals with diabetes and kidney disease make up the greatest proportion of persons requiring a kidney transplant or dialysis in Australia. Susceptibility to kidney disease in diabetes is not well understood, but previous studies have highlighted dysfunction of the power stations of the cells (mitochondria) as a potential mediator. In this project, we aim to better understand how dysfunction in mitochondria can contribute to kidney disease in diabetes. Our previous data has shown that changes in mitochondrial function happen early perhaps even as far back as at the diagnosis of diabetes. We know that a biomarker of mitochondrial function called mtDNA can tell us when this starts and how badly affected the power stations are and this aligns with early changes in kidney function. In this project, we will examine kidney and mitochondrial function in children and adolescents early in the development of diabetes. We will also look at where mtDNA comes from and if it can directly activate the immune system contributing to DKD.
Hypotheses: Mitochondrial damage early in diabetes can impact immune cell function contributing to the development of diabetic kidney disease.