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논문분류	춘계학술대회 초록집
제목	Ultra Long-Term Kidney Allograft Dysfunction Revealing Chronic Active T Cell Mediated Rejection After 28 Years
저자	Jiyae Yi
출판정보	2026; 2026(1):
키워드	Renal transplantation, Graft dysfunction, Chronic active T cell-mediated rejection, CA-TCMR, Immunosuppressant
초록	Case Study: Introduction Kidney allografts surviving beyond two decades are uncommon, and late graft dysfunction in ultra–long-term recipients is often attributed to non-immunologic causes such as aging, chronic calcineurin inhibitor toxicity, or interstitial fibrosis and tubular atrophy. Chronic active T cell–mediated rejection (CA-TCMR) occurring decades after transplantation is rarely reported and may be overlooked. We describe CA-TCMR developing 28 years after kidney transplantation, potentially triggered by brief immunosuppressant interruption and concurrent infection. Case Description A 60-year-old woman with end-stage kidney disease due to autosomal dominant polycystic kidney disease underwent living-unrelated donor kidney transplantation in December 1998. She maintained stable graft function for 28 years on cyclosporine, mycophenolic acid, and low-dose methylprednisolone, with baseline serum creatinine 1.1–1.4 mg/dL. Following international travel, she presented with fever, chills, myalgia, nausea, and vomiting. Laboratory evaluation showed elevated inflammatory markers and mild acute kidney injury (blood urea nitrogen 23.3 mg/dL, creatinine 2.26 mg/dL, C-reactive protein 4.26 mg/dL). After fluid resuscitation and empirical antibiotics, symptoms and renal function improved, and she was discharged. She was readmitted shortly thereafter with recurrent fever and worsening kidney function (blood urea nitrogen 54.4 mg/dL, creatinine 2.83 mg/dL). Further assessment revealed unintentional discontinuation of cyclosporine for three days during travel. Allograft biopsy demonstrated histologic findings consistent with chronic active T cell–mediated rejection. Conclusion CA-TCMR can occur even decades after transplantation. Brief immunosuppressive interruption, particularly with infection-related immune activation, may precipitate significant alloimmune injury. Careful adherence assessment and timely biopsy remain essential in evaluating late graft dysfunction.
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