Overview
Clinical Frame
Kidney allograft rejection is the central clinical model here, although other transplanted organs produce organ specific signs of graft dysfunction.
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.