Thrombotic microangiopathy (TMA) is a rare but serious medical disease that results in thrombosis in capillaries and arterioles due to an endothelial injury. It is a pattern of damage that can occur in the smallest blood vessels inside many of the bodys vital organs, most commonly the kidney and brain. TMA may be seen in association with thrombocytopenia, anemia, purpura, and kidney failure. The classic TMAs are hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Other conditions with TMA include atypical hemolytic uremic syndrome, disseminated intravascular coagulation, scleroderma renal crisis, malignant hypertension, antiphospholipid antibody syndrome, and drug toxicities.

The clinical presentation of TMA, although dependent on the type, typically includes fever, microangiopathic hemolytic anemia, kidney failure, thrombocytopenia, and neurological manifestations. Generally, renal complications are particularly predominant with Shiga-toxin-associated hemolytic uremic syndrome (STx-HUS) and atypical HUS, whereas neurologic complications are more likely with TTP. Individuals with milder forms of TTP may have recurrent symptomatic episodes, including seizures and vision loss. With more threatening cases of TMA, and also as the condition progresses without treatment, multi-organ failure or injury is also possible, as the hyaline thrombi can spread to and affect the brain, kidneys, heart, liver, and other major organs.

The course of treatment and the success rate is dependent on the type of TMA. Some patients with atypical HUS and TTP have been treated with plasma exchange, while others have been treated with eculizumab, a monoclonal antibody that blocks the complement system. Management of TMA associated with other secondary causes involves identifying and treating the underlying cause. Medication-induced TMA is initially managed by withdrawing the causative medication. The diagnosis of aHUS, which is caused by a dysregulation of the complement alternative pathway, is one of exclusion.