# Post-Transplant Complications > Post-transplant complications for NEET-SS Nephrology: infection timeline, CMV and BK virus, rejection types, PTLD and recurrent disease notes. - Canonical URL: https://prepelephant.com/topics/neet-ss/nephrology/post-transplant-complications - Exam / course: NEET-SS · Subject: Nephrology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Post-Transplant Complications", PrepElephant, https://prepelephant.com/topics/neet-ss/nephrology/post-transplant-complications ## 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.