Grant: Doctoral Award - Frederick Banting and Charles Best Canada Graduate Scholarships

Over 20 million people in North America (including 2 million Canadians) have chronic kidney disease. These individuals die from heart and blood vessel diseases more often than they need dialysis. This is due to hardening of the arteries caused by calcium deposits inside the blood vessel walls which is known as vascular calcification (VC). The calcium deposits damage the vessels, causing them to lose flexibility. This makes them unable to respond to the changing demands of the body. This will eventually lead to heart disease and death. The protein matrix Gla protein (MGP) is a potent inhibitor of VC. Vitamin K is a co-factor in the activation MGP and therefore adequate vitamin K stores are essential to inhibit calcification of the arteries. Population studies have shown that CKD patients develop more severe VC at a much younger age than the rest of the population. To date, the role of vitamin K and MGP have not yet been evaluated in an animal model of CKD. Our laboratory hypothesizes that vitamin K supplementation will slow the progression of CKD-induced VC and the associated changes in vascular properties. Warfarin is an anti-coagulation drug that is used widely in patients, including those with CKD, to prevent thrombosis. It acts by inhibiting vitamin K. Our laboratory hypothesizes that administration of therapeutic doses of warfarin will increase the progression of CKD-induced VC and the associated changes in vascular properties. Discovering the role of vitamin K and MGP carboxylation status in a CKD model will give us a further understanding of VC in CKD patients. This will allow for the development of better treatment for these patients, and a decrease in the morbidity and mortality as well as an increase in their quality of life.