Transplant Rejection, Teaching, and Long-Term Monitoring

A transplanted kidney can lose function because the recipient’s immune system recognizes donor tissue as foreign. The timing and mechanism of injury help predict the clinical picture and the treatment. Hyperacute rejection begins within minutes to hours. Preformed antibodies against the donor activate complement and damage the graft’s vessels, producing severe ischemia and immediate graft nonfunction. This is not treated with routine anti-rejection medication; the failed graft generally requires removal. Acute rejection can occur days to months after transplantation and may be either: - Cellular rejection, driven mainly by T lymphocytes attacking graft tissue. - Antibody-mediated rejection, in which donor-specific antibodies, or DSAs, injure the graft’s vascular endothelium. Acute rejection may cause fever, malaise, graft tenderness, reduced urine output, fluid retention, or hypertension, but symptoms can be absent. A rising serum creatinine may be the first detectable signal. Chronic rejection develops over months to years. Repeated immune injury, vascular narrowing, and fibrosis gradually reduce functioning nephron mass. The pattern is usually a slow decline in graft function, sometimes with increasing proteinuria. There is no reliably curative rescue once advanced chronic...