Chronic kidney disease is common but often underdiagnosed. About 10% of the population is estimated to have some form of kidney damage. Cardiovascular disease is much more common in people with kidney damage than in the general population and is the most common cause of death in kidney failure. Although the link between chronic kidney disease and cardiovascular disease has been known for over 100 years, the cause is not yet known. We have found in preliminary studies that the hormone Angiopoietin2, which if it reaches the circulation leads to pathological changes in blood vessels, is highly present in kidney tissue from rats with chronic kidney disease. Our hypothesis is that, in kidney disease, large amounts of this hormone are formed and released, leading to pathological changes in the blood vessels. We test our hypothesis in 3 steps. 1) We study the molecular mechanisms behind increased Angiopoietin2 production in kidney cells that are exposed to the stress of dealing with the increased amount of egg white secreted in the diseased kidney. 2) In rats with human kidney disease, we study the function, structure and amount of Angiopoietin2 in the kidney and vessels. 3) We study a group of young patients with chronic kidney disease with respect to the amount of Angiopoietin2 in blood and stiffness in arteries. If we succeed in identifying the molecular mechanism behind the link between chronic kidney disease and cardiovascular disease, this will enable the development of a targeted treatment to protect against the cardiovascular complications.