Our group uses experimental models to investigate mechanisms of vascular damage in chronic kidney disease and hypertension. One focus of our work is on the syndrome of “malignant hypertension” which is characterized by rapidly progressive target organ injury despite blood pressure levels which are very similar to those observed in non-malignant hypertension. Current projects address the role of defective angiogenic pathways in this syndrome. The second focus of our group is the impaired angiogenic response to ischemia in chronic kidney disease. Patients with chronic kidney disease suffer disproportionally from cardiovascular disease; stenosis or occlusions of arterial vessels occur more often, and the sequelae of these macrovascular events tend to be more severe than in patients with normal kidney function. We have previously shown that the angiogenic processes induced by ischemia (which are required to restore tissue perfusion) are impaired in an experimental model of chronic kidney disease (see figure). Current projects focus on therapeutic interventions to improve ischemia-induced angiogenesis in chronic kidney disease.