Research Awards Recipients

Lay Abstract

Diabetes is the primary cause of chronic kidney disease in Canada and is associated with a high mortality and significant cost to the health care system. Early detection can slow progression but at present very few treatments exist for individuals with chronic kidney disease. Because of this there is demand for new and more effective therapies for diabetic kidney disease. We have recently observed that a newly discovered immune signaling pathway, called neutrophil extracellular traps (NETs), is activated in animal models of diabetic kidney disease. This pathway is normally only activated in response to bacterial infection or autoimmune diseases such as Lupus. We believe that activation of this pathway in diabetes plays a key role in kidney injury. In the present study we will use cell and animal models to determine how NETs are formed in diabetes and how they cause injury to the kidney. We will then test if blocking NET formation prevents injury in an animal model of diabetic kidney disease. Our work addresses a top patient-identified research priority: "What are the most effective new interventions and treatments to prevent the development and progression of kidney disease?" Most drugs for individuals with kidney disease act on biological pathways that have been known for some time. However, until recently it was not known that NETs were important in the body. If we can understand how NETs are formed we may be able to identify new pathways for drug development.