Organ Rejection Medications

Anti-rejection medicines prevent immune injury from progressing, but the same immune suppression that protects a graft reduces the patient's ability to contain infection and may injure the kidneys, marrow, nervous system, or metabolism. The clinical task is therefore a balance: enough suppression to prevent rejection, without creating avoidable toxicity. Canadian transplant centres commonly use three complementary maintenance medicines—tacrolimus, mycophenolate mofetil, and a corticosteroid—for kidney, liver, and heart transplantation. The transplant team may alter the combination for organ type, time since transplant, comorbidities, or adverse effects. These medicines are not interchangeable, and a patient who feels well still needs them because rejection can begin before symptoms are obvious. Tacrolimus acts mainly on activated T cells. It inhibits calcineurin, which blocks IL-2 transcription and reduces T-cell activation. Mycophenolate mofetil inhibits inosine-5′-monophosphate dehydrogenase, depleting guanosine nucleotides needed for lymphocyte proliferation. Corticosteroids suppress inflammatory and immune signalling more broadly. Using different mechanisms allows the regimen to control alloimmune activity through several pathways rather than relying on one drug at a very toxic exposure.