Patients with kidney disease are significantly more likely than the general population to have angina, heart attacks, strokes and other diseases arising from damage to the arteries. Arteries are the pipes that distribute blood around the body. Indeed, most patients with kidney disease no longer die from the kidney disease itself, but from these diseases of the arteries. We are trying to understand why patients, even with relatively mild kidney disease, have an increased risk of these arterial conditions. It is known that most arterial disease results from narrowing of the arteries by a process called atherosclerosis, which involves the immune system. A heart attack or stroke can occur when a blood clot forms at the narrowing and blocks the artery. We are studying these processes in people with and without kidney disease. In particular we have a study in place looking at the function of platelets which are very important in the formation of the blood clots involved in heart attacks and strokes.
There is good evidence that patients with chronic kidney disease are at increased risk of cardiovascular disease, even when traditional risk factors such as hypertension and lipids have been taken into account. This applies to all stages of chronic kidney disease. We have recently identified a new receptor CLEC-2 on the surface of platelets and some immune cells. Triggering of this receptor causes potent platelet activation and aggregation, promoting thrombus formation, which is often the critical final step in myocardial infarction or stroke. Intriguingly, we have identified the ligand for this receptor and it is expressed in the kidney, suggesting a possible link between renal disease and cardiovascular disease. We are exploring the role of this molecule and its ligands on platelet function in people with and without chronic kidney disease. We are also studying the role of related molecules in the immune system on the process of atherosclerosis.