Transplant Rejection

Kidney allograft rejection is the central clinical model here, although other transplanted organs produce organ-specific signs of graft dysfunction. Rejection is immune injury to donor tissue, but a failing graft is not automatically being rejected. Calcineurin-inhibitor toxicity, BK virus nephropathy, infection, urinary obstruction, and vascular compromise can produce a similar creatinine rise and require very different treatment. Acute rejection follows two major patterns. T-cell-mediated rejection reflects recipient T lymphocytes attacking donor antigens. Antibody-mediated rejection reflects donor-specific anti-HLA antibodies activating complement. The distinction matters because intensifying immunosuppression may help rejection but worsen infection or BK nephropathy. A new, sustained change from a recipient’s graft-function baseline therefore calls for prompt transplant-team assessment, medication and adherence review, exclusion of dangerous mimics, and biopsy-guided treatment rather than an automatic increase in tacrolimus.