Transplant Rejection, Teaching, and Long-Term Monitoring

A kidney allograft is vulnerable to immune injury because the recipient’s immune system recognises donor tissue as foreign. The timing of graft dysfunction gives an initial clue about the mechanism, but the categories overlap enough that treatment should never be chosen from timing alone. Hyperacute rejection occurs within minutes to hours. Preformed antibodies rapidly injure the graft’s blood vessels, producing severe vascular damage and loss of perfusion. This is a graft emergency; there is no treatment that reliably reverses the process, and graft removal is generally required. Acute rejection occurs days to months after transplant and may be either: - Cellular-mediated rejection, in which T lymphocytes attack donor antigens. This is usually treated first with high-dose corticosteroids. - Antibody-mediated rejection, in which donor-specific antibodies injure the graft, particularly its vascular endothelium. This requires antibody-directed treatment rather than steroids alone. Fever, malaise, graft tenderness, reduced urine output, and a rising serum creatinine can accompany acute rejection. The absence of pain or fever does not exclude it; a change in kidney function may be the first and only clue. Chronic rejection develops...