What is a major consequence of hyperacute transplant rejection?

Hyperacute transplant rejection is a rapid and immediate response that occurs typically within minutes to hours after transplantation, primarily due to pre-existing recipient antibodies against donor antigens, which is often a result of previous sensitization through blood transfusions or prior transplants.

In this context, the formation of fibrin thrombi in capillaries is the defining feature of hyperacute rejection. When antibodies bind to the endothelium of the graft, they initiate a type of immune response that leads to complement activation and recruitment of inflammatory mediators. This cascade results in increased vascular permeability and fibrin deposition in the microvasculature of the graft, forming thrombi and ultimately causing occlusion of these blood vessels, which impairs blood supply to the graft.

The immediate consequences of this process manifest as a pallor or cyanosis of the graft, and it can lead to rapid graft failure if not promptly addressed. Other immune mechanisms such as lymphocyte infiltration or necrosis may be observed in different types of rejection (e.g., acute or chronic rejection) but are not characteristic of hyperacute rejection. In summary, the presence of fibrin thrombi is a hallmark of the early, destructive immune response that typifies hyperacute transplant rejection.