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Abstract: SA-PO1221

BK Virus Nephropathy and Drug-Induced Interstitial Nephritis After Deceased Donor Lung Transplantation for Lymphangioleiomyomatosis

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Tanaka, Shin, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Kadota, Nozomi, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Takagi, Miyuki, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Saeki, Harumi, Department of Human Pathology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Gohda, Tomohito, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Seyama, Kuniaki, Division of Respiratory Medicine, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Suzuki, Yusuke, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
Introduction

Renal dysfunction is a common complication after non-renal solid organ transplantation and is associated with poor prognosis. Its causes include nephrotoxicity related to calcineurin inhibitors (CNIs) and mTOR inhibitors, perioperative hemodynamic injury, metabolic complications, and infections. BK virus nephropathy (BKVN), a well-recognized cause of graft dysfunction after kidney transplantation, is rare in non-renal solid organ transplant recipients, and no established treatment strategy currently exists.

Case Description

Ten years before transplantation (X −10), the patient was diagnosed with sporadic lymphangioleiomyomatosis (LAM) and started treatment with sirolimus, an mTOR inhibitor. In February of year X, the patient underwent deceased-donor right single-lung transplantation with an eGFR of 90 mL/min/1.73 m2. Post-transplant immunosuppressive therapy consisted of prednisolone, tacrolimus, and mycophenolate mofetil (MMF). In January of X+2, MMF was discontinued because of cytomegalovirus enteritis, and sirolimus, which had also been used to treat the underlying disease, was resumed. Renal function, which had remained stable at an eGFR of approximately 70 mL/min/1.73 m2 after transplantation, gradually declined and reached 25 mL/min/1.73 m2 by X+4. A kidney biopsy was therefore performed in January of X+5. Renal histopathology revealed thrombotic microangiopathy, tubulointerstitial nephritis, tubulitis, and arteriolar hyalinosis. In addition, SV40-positive nuclei were identified in tubular epithelial cells. Based on these findings, the patient was diagnosed with BK virus nephropathy accompanied by drug-induced tubulointerstitial nephritis associated with both mTOR inhibitor and calcineurin inhibitor exposure.

Discussion

We report a case of BK virus nephropathy and drug-induced tubulointerstitial nephritis that developed after reintroduction of an mTOR inhibitor following lung transplantation. The switch from MMF to sirolimus, together with continued tacrolimus exposure, may have contributed to progressive renal dysfunction. Careful adjustment of immunosuppressive therapy and comprehensive long-term management are essential for preservation of both allograft and native kidney function.