A model of the parallel pathogenic processes in HUS. Excess complement activation on endothelial cell, platelet, and red cell surfaces leads to C5a release and membrane attack complex (MAC) formation. This leads to enhanced tissue factor (TF) activity on the endothelium, activation and aggregation of platelets, and release of hemoglobin and reduction of nitric oxide (NO) in plasma. These phenomena lead to a procoagulative state, coagulation, and thrombosis-mediated tissue damage. There are several feedback loops in this process. These loops can be seen as a cycle that may be initiated at several points and where several phenomena may take place in parallel. This may explain why STEC-HUS, secondary HUS, and aHUS share clinical features although the processes start in various ways. DGKε, diacylglycerol kinase ε.