Transplant Rejection, Teaching, and Long-Term Monitoring

A kidney allograft can fail because of rejection, but the pattern of failure depends on the immune mechanism and the time course. Hyperacute rejection occurs within minutes to hours when pre-existing recipient antibodies recognize donor antigens. Complement activation and thrombosis rapidly destroy graft perfusion. The kidney may become immediately nonfunctional. This is a transplant emergency; irreversible vascular injury may require urgent graft removal rather than observation. Acute cellular rejection is driven by recipient T-cell activation against donor HLA antigens. It commonly appears during the early post-transplant period but can occur later, especially when immunosuppressant exposure is inadequate. The clinical signal is often a new or progressive rise in serum creatinine, with or without fever, malaise, graft tenderness, reduced urine output, fluid retention, or hypertension. Symptoms can be muted by immunosuppression. Antibody-mediated rejection results from antibodies directed against the allograft, often donor-specific antibodies. Severe disease may present with rapidly worsening graft function and requires urgent treatment because delay can lead to irreversible injury. Chronic allograft dysfunction develops over months to years as persistent immune and nonimmune injury produces gradual loss of...