Transplant Rejection, Teaching, and Long-Term Monitoring

Rejection is immune-mediated injury to a transplanted kidney. The timing and pattern help identify the likely process, but laboratory trends and tissue diagnosis determine what is actually happening. Hyperacute rejection develops within minutes to hours, usually because antibodies already present in the recipient recognize donor antigens. Complement activation causes severe vascular injury and graft ischemia. The kidney may become painful, swollen, and nonfunctional almost immediately; urgent graft removal is usually required because the injury is not reversible. Acute cellular rejection is driven by recipient T-cell activation against donor HLA antigens. It commonly appears days to months after transplantation but can occur later, particularly when immunosuppression is interrupted or reduced. A rising serum creatinine is often the first meaningful clue. Decreased urine output, graft tenderness, fever, malaise, new or worsening hypertension, edema, or weight gain may accompany it, but rejection can be clinically silent. Chronic allograft injury evolves over months to years. Progressive vascular and interstitial damage gradually reduces graft function. The patient may have few symptoms while creatinine rises and eGFR declines. Chronic dysfunction is not diagnosed from one abnormal...