Synopsis
Assess acute kidney-allograft dysfunction without anchoring, recognise infection despite blunted signs, and protect both patient and graft through immediate transplant-centre coordination.
- An allograft creatinine rise has a broad differential: rejection, infection, hypovolaemia, obstruction, vascular compromise, calcineurin toxicity, recurrent disease and other AKI causes.
- Contact the patient's transplant centre early; timing, induction regimen, donor-recipient virology, previous rejection, antibodies and usual creatinine change interpretation.
- Rejection may be asymptomatic and is not reliably distinguished from infection or tacrolimus toxicity by examination or creatinine pattern alone.
Key red flags
A reproducible creatinine rise, new proteinuria or falling urine output may be the only rejection sign; normal temperature and a non-tender graft do not make it benign.
Investigation priorities
Quantify allograft dysfunction and detect dialysis-threatening complications.
Management branches
Creatinine exceeds the recipient's established baseline or urine output falls.
- Contact the transplant centre, confirm timeline, baseline, adherence, recent illness and interacting medicines, and assess ABCDE, fluid state, blood pressure and urine output.
- Obtain electrolytes, cultures, urinalysis, drug trough, viral PCR and urgent ultrasound-Doppler according to presentation, treating sepsis or life-threatening electrolyte disturbance immediately.
Key medicines
Tacrolimus maintenance immunosuppressionUse the recipient-specific immediate- or modified-release oral regimen at fixed times, adjusted only by the transplant team to a correctly timed trough target that varies with post-transplant stage and immune risk.
Mycophenolate mofetilUse the transplant-centre twice-daily oral dose, commonly 1 g twice daily initially in adults, reduced or interrupted only for protocol-defined toxicity, infection or reproductive planning under specialist direction.