Medicina Bucureşti

Hyperacute rejection occurs when preformed antidonor antibodies are present in the circulation of the recipient. Such antibodies may be present in a recipient who has already rejected a kidney transplant. Multiparous women who develop anti-HLA antibodies against paternal antigens shed from the fetus may also have preformed antibodies to grafts taken from their husbands or children. Prior blood transfusions from HLA-nonidentical donors can also lead to presensitization because platelets and white cells are particularly rich in HLA antigens. In such circumstances, rejection occurs immediately after transplantation because the circulating antibodies react with and deposit rapidly on the vascular endothelium of the grafted organ. Complement fixation occurs, and an Arthus-type reaction follows.

This form of rejection occurs within minutes or hours after transplantation and can sometimes be recognized by the surgeon just after the graft vasculature is anastomosed to the recipient's. In contrast to the nonrejecting kidney graft, which rapidly regains a normal pink coloration and normal tissue turgor and promptly excretes urine, a hyperacutely rejecting kidney rapidly becomes cyanotic, mottled, and flaccid and may excrete a mere few drops of bloody urine. The histologic lesions are characteristic of the classic Arthus reaction. There is a rapid accumulation of neutrophils within arterioles, glomeruli, and peritubular capillaries. Immunoglobulin and complement are deposited in the vessel wall, and electron microscopy discloses early endothelial injury together with fibrin-platelet thrombi. These early lesions point to an antigen-antibody reaction at the level of vascular endothelium. Subsequently, these changes become diffuse and intense, the glomeruli undergo thrombotic occlusion of the capillaries, and fibrinoid necrosis occurs in arterial walls. The kidney cortex then undergoes outright infarction (necrosis), and such nonfunctioning kidneys are removed.

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