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.
- Fever and inflammatory responses can be muted by immunosuppression, so confusion, hypotension, breathlessness, diarrhoea or unexplained graft dysfunction may be the infection signal.
- Urinary infection may lack dysuria or graft pain because the allograft is denervated; obtain cultures before antibiotics when this does not delay sepsis care.
- Early infection is often surgical or healthcare-associated; later opportunistic risk includes CMV, BK polyomavirus and Pneumocystis, shaped by prophylaxis and net immunosuppression.
- Ultrasound with Doppler assesses hydronephrosis, collections and major vascular flow but cannot rule out cellular or antibody-mediated rejection.
- Allograft biopsy usually establishes rejection type, while donor-specific antibody testing supports antibody-mediated disease and guides centre-specific treatment.
- Tacrolimus has a narrow therapeutic range and major azole, macrolide, anticonvulsant, herbal and grapefruit interactions; measure a correctly timed trough and call renal pharmacy.
- BK nephropathy treatment commonly requires supervised immunosuppression reduction, whereas rejection requires intensification; guessing between them can damage the graft.
- Keep prophylaxis, vaccination and reproductive plans current; live vaccines are generally avoided during clinically significant immunosuppression and mycophenolate is a major teratogen.
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.
Hypotension, tachypnoea, confusion, hypoxia, rigors or lactate elevation can occur with little fever or leukocytosis and requires immediate cultures, antimicrobials and transplant advice.
Oliguria, anuria, graft swelling, haematuria, new hypertension, bruit or abrupt severe dysfunction raises obstruction, leak, collection, artery stenosis or thrombosis and needs urgent imaging.
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.
- If no rapidly reversible cause explains dysfunction, arrange transplant-team biopsy and DSA testing; do not give empirical rejection steroids before infection and histology discussion unless directed.