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Published on: October 16, 2018
BK Virus Nephropathy Associated With Prolonged Immune Effector Cell-Associated Hematotoxicity Following Anti-CD19
Naoto Okubo1, Hanae Wakabayashi1, Daisuke Honda1
1Department of Nephrology, Chiba University Hospital, Chiba, Japan.
We report the case of a 67-year-old Japanese woman with diffuse large B-cell lymphoma who developed BK virus nephropathy (BKVN) following anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy. CAR-T therapy is an effective treatment for certain refractory hematologic malignancies; however, immune effector cell-associated hematotoxicity often presents as a clinical complication. Our patient developed progressive kidney dysfunction 6 months after CAR-T therapy in the setting of prolonged immune effector cell-associated hematotoxicity. BK viral DNA was detected in both the blood and urine, and kidney biopsy showed focal tubulointerstitial nephritis with simian virus 40 positivity in tubular epithelial cells, consistent with a BKVN diagnosis. Intravenous immunoglobulin (2 g/kg) was administered. The serum creatinine level and BK viral load continuously increased, possibly because of the delayed treatment. BKVN is a common complication in kidney transplant recipients but uncommon in nontransplant patients. As no established treatment for BKVN in nontransplant patients is currently available, early detection is crucial. To our knowledge, this is the first reported case of BKVN after CAR-T therapy. Routine monitoring for BK virus infection should be considered in patients experiencing prolonged myelosuppression after CAR-T therapy to enable early detection and prompt management of BKVN.
We report the case of a 67-year-old Japanese woman with diffuse large B-cell lymphoma who developed BK virus nephropathy (BKVN) following anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy. CAR-T therapy is an effective treatment for certain refractory hematologic malignancies; however, immune effector cell-associated hematotoxicity often presents as a clinical complication. Our patient developed progressive kidney dysfunction 6 months after CAR-T therapy in the setting of prolonged immune effector cell-associated hematotoxicity. BK viral DNA was detected in both the blood and urine, and kidney biopsy showed focal tubulointerstitial nephritis with simian virus 40 positivity in tubular epithelial cells, consistent with a BKVN diagnosis. Intravenous immunoglobulin (2 g/kg) was administered. The serum creatinine level and BK viral load continuously increased, possibly because of the delayed treatment. BKVN is a common complication in kidney transplant recipients but uncommon in nontransplant patients. As no established treatment for BKVN in nontransplant patients is currently available, early detection is crucial. To our knowledge, this is the first reported case of BKVN after CAR-T therapy. Routine monitoring for BK virus infection should be considered in patients experiencing prolonged myelosuppression after CAR-T therapy to enable early detection and prompt management of BKVN.
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