Abstract
Since the first descriptions of haemolytic-uremic syndrome (HUS) by Moschowitz and thrombotic thrombocytopenic purpura (TTP) by Gasser, our knowledge about thrombotic microangiopathy (TMA) has grown considerably [1]. TMA now refers to a group of diseases comprising mechanical hemolytic anemia, peripheral thrombocytopenia, and varying degrees of organ failure. The incidence of TMA is increasing in the USA. Considerable progress has recently been made in the understanding of the pathophysiological mechanisms of TMA. These rare diseases, characterized by platelet thrombi in the microcirculation, are responsible for often serious organ dysfunction leading to the admission of these patients to intensive care units (ICUs). The prognosis of TMA was extremely poor prior to plasma therapy and especially plasma exchange. TMA is a serious, life-threatening disease that requires early diagnosis and urgent specialized therapeutic management.