Chieh-Li Yen1, Ya-Chung Tian1, Hsin-Hsu Wu2, Cheng-Hao Weng2, Yung-Chang Chen1, Kun-Hua Tu2, Shou-Hsuan Liu2, Cheng-Chia Lee2, Ping-Chin Lai1, Ji-Tseng Fang1, Cheng-Chieh Hung1, Chih-Wei Yang1, Yi-Jung Li3. 1. Kidney Research Center, Department of Nephrology, Linkou Chang Gung Memorial Hospital, Taipei, Taiwan; Department of Medicine, Chang Gung University, Taoyuan, Taiwan. 2. Kidney Research Center, Department of Nephrology, Linkou Chang Gung Memorial Hospital, Taipei, Taiwan; Department of Medicine, Chang Gung University, Taoyuan, Taiwan; Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan. 3. Kidney Research Center, Department of Nephrology, Linkou Chang Gung Memorial Hospital, Taipei, Taiwan; Department of Medicine, Chang Gung University, Taoyuan, Taiwan; Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan. Electronic address: r5259@cgmh.org.tw.
Abstract
BACKGROUND/ PURPOSE: Polyomavirus BK (BKV) reactivation causes allograft dysfunction in some kidney transplant recipients. The use of mammalian target of rapamycin (mTOR) inhibitor-based immunotherapy is associated with a lower incidence of polyomavirus-associated nephropathy compared with other immunosuppressants. This retrospective study assessed whether conversion to mTOR inhibitor-based immunotherapy directly reduced urinary BKV load. METHODS: A total of 63 kidney recipients were divided into mTOR inhibitor-conversion (21 patients) and nonconversion (42 patients) groups. Urinary BKV loads were determined before and at least 6 months after the conversion. RESULTS: The results demonstrated that urinary BKV titer was significantly reduced in the conversion group (3.94 ± 0.43 copies (log)/mL to 2.49 ± 0.19 copies (log)/mL) and remained unaltered in the nonconversion group (3.19 ± 0.20 copies (log)/mL to 2.90 ± 0.20 copies (log)/mL). In addition, the percentage of patients with reduced urinary BKV load was significantly higher in the conversion group (76.2% vs. 42.9%). The estimated glomerular filtration rate after 24 months mTOR inhibitor conversion was significantly increased compared with that in the nonconversion group. Conversion to mTOR-inhibitor-based immunotherapy was the only factor associated with an increase in estimated glomerular filtration rate. CONCLUSION: This study reveals an association of conversion to mTOR-inhibitor-based immunotherapy with the reduction of urinary BKV load.
BACKGROUND/ PURPOSE:Polyomavirus BK (BKV) reactivation causes allograft dysfunction in some kidney transplant recipients. The use of mammalian target of rapamycin (mTOR) inhibitor-based immunotherapy is associated with a lower incidence of polyomavirus-associated nephropathy compared with other immunosuppressants. This retrospective study assessed whether conversion to mTOR inhibitor-based immunotherapy directly reduced urinary BKV load. METHODS: A total of 63 kidney recipients were divided into mTOR inhibitor-conversion (21 patients) and nonconversion (42 patients) groups. Urinary BKV loads were determined before and at least 6 months after the conversion. RESULTS: The results demonstrated that urinary BKV titer was significantly reduced in the conversion group (3.94 ± 0.43 copies (log)/mL to 2.49 ± 0.19 copies (log)/mL) and remained unaltered in the nonconversion group (3.19 ± 0.20 copies (log)/mL to 2.90 ± 0.20 copies (log)/mL). In addition, the percentage of patients with reduced urinary BKV load was significantly higher in the conversion group (76.2% vs. 42.9%). The estimated glomerular filtration rate after 24 months mTOR inhibitor conversion was significantly increased compared with that in the nonconversion group. Conversion to mTOR-inhibitor-based immunotherapy was the only factor associated with an increase in estimated glomerular filtration rate. CONCLUSION: This study reveals an association of conversion to mTOR-inhibitor-based immunotherapy with the reduction of urinary BKV load.