ABO-incompatible Organ Transplantation by Yi Wang

Author:Yi Wang
Language: eng
Format: epub, pdf
ISBN: 9789811333996
Publisher: Springer Singapore

1.1 Hyperacute Rejection

Hyperacute rejection is termed as the rejection response which develops within few minutes to the first 24 h after bloodstream is opened to the allograft. This type of rejection is most commonly seen in second transplantation cases and recipients with history of repeated blood transfusion, multiple gestations, long-term hemodialysis, and/or multiple organ transplants. It is caused by the preexisting antibodies against alloantigen from recipients including ABO hemagglutinin, platelet antigen, HLA, as well as VEC antigens, belonging to type III hypersensitivity reactions. Once antigen-antibody complex is formed, complement system is activated which can destroy target cells directly and activate cascade to increase permeability of vasculature and neutrophil infiltration by bioactive fragments, finally leading to severe capillary and vascular endothelial injuries along with fibrin deposit and platelet aggregation. The outcome of this process is an irreversible catastrophic allograft damage which is characterized by diffuse arteritis, thrombosis, and massive tissue necrosis.

Aside from the immunological causes, sub-optimally infused organ and long ischemia time may also attribute to the development of hyperacute rejection.

Clinical and pathological manifestations: Hyperacute rejection is an irreversible humoral response. On gross examination, shortly after restoration of blood supply, the color of transplanted organ gradually turns out from bright red to dark red or blue. The consistency is also softened with possible hemorrhagic necrosis, enlarged size, and mottled appearance. Biopsy findings may include small vessel vasculitis with thrombosis formation, neutrophil infiltration, and fibrinoid necrosis of vascular wall as well as the presence of IgG, IgM, and complements.

Diagnosis and management: It is important to have surgical situations on the list of differential diagnosis, which include blood vessel tortuosity, arterial or venal thrombi, anastomosis stricture, or hypotension of the recipient. These factors may cause perfusion impairment and allograft injury which is similar to hyperacute rejection. Since hyperacute rejection is an irreversible, rapid, and intense immunological response, physicians should prevent its onset with their best effort. Nowadays, the measures to prevent hyperacute rejection include preconditioning with immunosuppressants before surgery, ABO typing and HLA matching, and crossmatch testing between the donor and recipient to exclude the presence of preformed donor-specific antibodies [2]. PRA test and CTL can provide information of recipient’s sensitization status and HLA antibody level. Plasmapheresis and immunoglobulin infusion can be effective on ameliorating hyperacute rejection when recognized at early stage, but resection of the allograft is inevitable in most instances to prevent further lethal complications.

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