Kidney Week

Abstract: PUB230

Chronic Active T-Cell-Mediated Rejection (CA-TCMR) After 28 Years of Stable Kidney Allograft Function

Session Information

• Publication Only

Category: Transplantation

• 2002 Transplantation: Clinical

Authors

• Yi, Jiyae, Bongseng Memorial Hospital, Busan, Korea (the Republic of)

Jiyae Yi, MD

• Kim, Joong Kyung, Bongseng Memorial Hospital, Busan, Korea (the Republic of)

Joong Kyung Kim, MD

• Oh, Joon Seok, Bongseng Memorial Hospital, Busan, Korea (the Republic of)

Joon Seok Oh, MD, PhD

• Ahn, Jeongmyung, Bongseng Memorial Hospital, Busan, Korea (the Republic of)

Jeongmyung Ahn, MD

• Kim, Hee yeoun, Bongseng Memorial Hospital, Busan, Korea (the Republic of)

Hee yeoun Kim, MD

• Kim, Yanghyeon, Bongseng Memorial Hospital, Busan, Korea (the Republic of)

Yanghyeon Kim, MD

• Lee, A Rim, Bongseng Memorial Hospital, Busan, Korea (the Republic of)

A Rim Lee, DO, DrMed, DrPH

Introduction

CA-TCMR developing decades after kidney transplantation is rarely recognized in ultra–long-term allograft survivors. We report biopsy-proven CA-TCMR occurring 28 years after transplantation following temporary calcineurin inhibitor interruption.

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 1998. She maintained stable graft function for 28 years on cyclosporine, mycophenolic acid, and low-dose methylprednisolone, without prior rejection episodes.
After overseas travel, she presented with 3 days of myalgia, nausea, diarrhea, and cough. Laboratory evaluation showed acute kidney injury and systemic inflammation (BUN 23.3 mg/dL, Cr 2.26 mg/dL, CRP 4.26 mg/dL). Suspected gastroenteritis with volume depletion improved with intravenous fluids and supportive care, and she was discharged with partial renal recovery (Cr 1.73 mg/dL).
Ten days later, she was readmitted with worsening graft dysfunction (BUN 43.3 mg/dL, Cr 2.47 mg/dL). Cyclosporine trough level was 59.6 ng/mL, and urinalysis showed microscopic hematuria and proteinuria. Kidney allograft biopsy revealed CA-TCMR, Banff grade IA, with focal pyelonephritis (t2, ci3, ct3, cv2, i-IFTA2, t-IFTA2, ti2, C4d0).
Further history revealed interruption of cyclosporine therapy for 5 days during travel. Intravenous methylprednisolone pulse therapy (500 mg daily for 4 days) was administered. Additional immunosuppression was deferred because of advanced chronic histologic injury and the patient’s condition. She was discharged with persistent graft dysfunction (Cr 2.87 mg/dL).

Discussion

This case demonstrates that clinically significant CA-TCMR may develop even after decades of stable graft function. Brief interruption of maintenance immunosuppression, particularly in the setting of concurrent infection or immune activation, can trigger late alloimmune injury, highlighting the importance of adherence assessment and timely biopsy in late graft dysfunction.

PAS showing severe IF/TA with chronic vasculopathy and ongoing inflammation