What is the primary cause of small renal vessel occlusion in Hemolytic Uremic Syndrome (HUS)?

In the context of Hemolytic Uremic Syndrome (HUS), small renal vessel occlusion is primarily caused by the deposition of fibrin, which results from a cascade of events instigated by endothelial injury. This injury is often triggered by Shiga toxin produced by certain strains of Escherichia coli. This toxin damages the endothelial cells of the glomeruli, leading to an inflammatory response and the activation of the coagulation cascade. As a result, fibrin is deposited in the renal microvasculature.

The deposition of fibrin is central to the pathophysiological changes observed in HUS. It contributes to the formation of microthrombi and reduces blood flow to the renal tissues, leading to the characteristic clinical manifestations of kidney dysfunction, hemolytic anemia, and thrombocytopenia. Thus, the occlusion of small renal vessels is primarily related to this fibrin deposition rather than the direct effects of the toxin or the initial infection itself.