Post-Transplant Complications
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Direct answer
The month count since transplantation predicts the culprit better than any single investigation. The first month belongs to surgical complications — urine leaks, lymphocele, ureteric stenosis — plus donor-derived infection and delayed graft function. Months one to six are the arena of acute rejection and the classic opportunists: cytomegalovirus, which strikes hardest in the donor-positive recipient-negative pairing, and BK virus, which climbs from viruria to viraemia to nephropathy and mimics rejection precisely. Beyond six months the threats become chronic rejection, recurrent primary disease, and post-transplant lymphoproliferative disorder. A rising creatinine is therefore never interpreted without asking how many months out the patient is.
What you must remember
- Timeline skeleton: under one month — surgical and technical; one to six months — acute rejection, CMV, BK; beyond six months — chronic rejection, recurrent disease, PTLD, community infections.
- CMV: donor-positive recipient-negative carries the highest risk; prophylaxis with valganciclovir for three to six months; tissue-invasive disease involves the gut, lung and retina; treatment is therapeutic-dose valganciclovir.
- BK virus: viruria, then viraemia above roughly 10,000 copies per millilitre, then nephropathy; management is measured reduction of immunosuppression — there is no proven antiviral, and the biopsy closely mimics acute rejection.
- Acute cellular rejection: Banff-scored tubulitis and interstitial inflammation; first-line is pulsed methylprednisolone, with antithymocyte globulin for steroid-resistant disease.
- Antibody-mediated rejection: donor-specific antibodies, C4d staining of peritubular capillaries and glomerulitis; treated with plasmapheresis, intravenous immunoglobulin and rituximab.
- PTLD: Epstein–Barr virus-driven B-cell proliferation, commonest in the first year and in donor-positive recipient-negative children; first move is reduction of immunosuppression, then rituximab-based therapy.
- Recurrent disease: focal segmental glomerulosclerosis recurs earliest — nephrotic-range proteinuria within hours to days of implantation; primary hyperoxaluria mandates combined liver-kidney transplantation.
- Indian programme reality: tuberculosis reactivation is a leading opportunistic infection after transplantation in India, so latent tuberculosis screening — and treatment before or alongside immunosuppression — is standard practice.
A creatinine that rises at month two
A 45-year-old recipient, two months past a deceased-donor kidney on tacrolimus and mycophenolate, phones in with a creatinine that has crept from 1.2 to 1.8 mg/dL. Step one: exclude the trivial and the mechanical — is he dehydrated, has he missed doses, and what does the ultrasound say about hydronephrosis, collections and resistive indices? Step two: check the tacrolimus trough, because calcineurin nephrotoxicity and rejection present with the identical number. Step three: infection screen — BK plasma PCR and CMV PCR on the same draw; a BK viral load above 10,000 copies per millilitre with tubulointerstitial changes on biopsy is BK nephropathy, and the treatment is the opposite of what rejection would demand: taper, do not intensify. Step four: if the screen is negative, biopsy — Banff tubulitis secures acute cellular rejection and pulsed steroids follow; peritubular capillary C4d with donor-specific antibodies redefines the case as antibody-mediated and brings plasmapheresis. Step five: revisit history — a recent azole or rifampicin prescription is as plausible an answer as any biopsy finding, which is the lesson the timeline teaches: at month two, the differential is drug, virus or rejection, in that order of cheapness to test.
How the exam frames it
Stems in this pool are built on pattern recognition across the timeline. Sterile pyuria with a rising creatinine is the classic BK vignette; a donor-positive recipient-negative recipient with fever, diarrhoea and hepatitis at month three is CMV until the PCR says otherwise; a paediatric recipient with fever and lymphadenopathy in the first year is PTLD until the biopsy says so. The recurrent-disease question is timed too — nephrotic-range proteinuria on day two after transplantation means recurrent focal segmental glomerulosclerosis and plasmapheresis, a favourite answer because it is the one complication that begins within hours. Indian papers add the tuberculosis angle: a transplant recipient with fever and weight loss at any month earns a tuberculosis work-up before a lymphoma work-up, because post-transplant tuberculosis in the Indian setting outnumbers PTLD several-fold.
Frequently asked questions
Which transplant pairing carries the highest CMV risk?
Donor seropositive, recipient seronegative — managed with valganciclovir prophylaxis for three to six months.
How is BK virus nephropathy managed?
By measured reduction of immunosuppression, with screening viral loads; no antiviral is of proven benefit, and intensifying immunosuppression for presumed rejection worsens it.
What marks antibody-mediated rather than cellular rejection?
Donor-specific antibodies with C4d deposition in peritubular capillaries and glomerulitis on biopsy; plasmapheresis, immunoglobulin and rituximab form the treatment backbone.
When should PTLD be suspected?
Unexplained fever, lymphadenopathy or weight loss — chiefly in the first year and in Epstein–Barr virus-mismatched recipients; reduce immunosuppression first, then treat as lymphoma.
Which native disease recurs within hours of transplantation?
Primary focal segmental glomerulosclerosis — immediate massive proteinuria treated urgently with plasmapheresis and rituximab.
Why is tuberculosis screening routine in Indian transplant programmes?
Immunosuppression sharply raises reactivation risk in a high-prevalence population, so latent infection is sought and treated before or alongside transplantation.