Chronic kidney disease often leads to kidney failure. We study four kidney diseases: Hemolytic Uremic Syndrome (HUS), Thrombotic Thrombocytopenic Purpura (TTP), vasculitis and IgA nephropathy. HUS is characterized by low platelets, anemia and acute renal failure. There are two variants. Typical HUS is caused by intestinal infection with enterohemorrhagic Escherichia coli (EHEC) bacteria. There was a very large outbreak in Europe in May-June 2011. Atypical HUS is associated with gene mutations in complement proteins, part of the innate defense system. This activates the complement system and attacks the body's own cells. TTP involves a mutation in ADAMTS13, a plasma enzyme that cleaves von Willebrand factor within the blood's delivery system. This leads to the formation of blood clots. TTP patients have the same symptoms as HUS including fever and neurological symptoms. Vasculitis is characterized by inflammation of blood vessels that affects the blood supply to several organs, especially the kidneys. The cause is unknown but the body's own white blood cells and the immune system play a crucial role. IgA nephropathy is the most common form of kidney inflammation in the Western world. It can be triggered by upper respiratory tract infections. Our studies aim to identify the molecular mechanisms behind these diseases, both bacterial and host factors. We aim to map how the body's cells are affected, how blood cells are activated and vessels are damaged, in order to develop specific treatments that are currently lacking.