Immunosuppression and Rejection Management
Core concepts
Master induction (basiliximab, antithymocyte globulin, alemtuzumab) and maintenance regimens combining a calcineurin inhibitor, an antimetabolite, and corticosteroids. Know mechanisms, toxicities, and monitoring: tacrolimus and cyclosporine levels, mycophenolate gastrointestinal and teratogenic effects, and corticosteroid metabolic effects. Understand rejection classification: hyperacute, acute cellular, acute antibody-mediated, and chronic (including chronic lung allograft dysfunction and transplant glomerulopathy). Learn diagnosis by biopsy with Banff grading, donor-specific antibody testing, and C4d staining. Know treatment: pulse steroids for cellular rejection, plasma exchange and intravenous immunoglobulin plus rituximab for antibody-mediated rejection, and reduction of immunosuppression when infection competes.
Traps
Questions confuse therapeutic drug monitoring targets: tacrolimus troughs differ by phase and organ. Another trap is treating a rising creatinine with steroids before excluding infection or obstruction. Distinguish de novo donor-specific antibody from preformed antibody. Remember that calcineurin inhibitor nephrotoxicity can mimic rejection, and that antibody-mediated rejection may occur with negative C4d in some settings.
Worked example
A lung recipient with declining forced expiratory volume in one second and new donor-specific antibody. Rule of thumb: evaluate for chronic lung allograft dysfunction phenotype and antibody-mediated rejection; treatment may include antibody-directed therapy plus adjustment of maintenance immunosuppression, not steroids alone.
Study strategy
Create a drug table of mechanism, monitoring, and signature toxicity, then pair each rejection type with its diagnostic test and first-line therapy.