Emily M Eichenberger, Wairimu Magua, Joseph B Rickert, Geeta Karadkhele, Mohammad Kazem Fallahzadeh, Payaswini Vasanth, Christian Larsen
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Three BKPyV-dyn states were defined: BKPyV-dyn1 (viral load <3 log<sub>10</sub>), BKPyV-dyn2 (viral load ≥ 3 log<sub>10</sub> and ≤4 log<sub>10</sub>), and BKPyV-dyn3 (viral load >4 log<sub>10</sub>).</p><p><strong>Results: </strong>Two hundred eighty KTR on belatacept- and 280 KTR on tacrolimus-based regimens were compared. The probability of transitioning between BKPyV-dyn states and time spent in each state in both groups was comparable. Total duration in BKPyV-dyn-1 was 632.1 days (95% CI 612.1, 648.5) for belatacept versus 615.2 days (95% CI 592.5, 635.8) for tacrolimus, BKPyV-dyn-2 was 49.2 days (95% CI 41.3, 58.4) for belatacept versus 55.6 days (95% CI 46.5, 66.8) for tacrolimus, and BKPyV-dyn-3 was 48.7 days (95% CI 37.1, 363.1) for belatacept versus 59.2 days (95% CI 45.8, 73.5) for tacrolimus. BKPyV associated nephropathy (PyVAN) occurred in 3.9% in belatacept- and 3.9% tacrolimus-treated KRT (P > .9).</p><p><strong>Conclusions: </strong>Compared with tacrolimus-based immunosuppression, belatacept based immunosuppression was not associated with increased risk of BKPyV-DNAemia or nephropathy.</p>","PeriodicalId":23318,"journal":{"name":"Transplant Infectious Disease","volume":" ","pages":"e14298"},"PeriodicalIF":2.6000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Belatacept-based immunosuppression does not confer increased risk of BK polyomavirus-DNAemia relative to tacrolimus-based immunosuppression.\",\"authors\":\"Emily M Eichenberger, Wairimu Magua, Joseph B Rickert, Geeta Karadkhele, Mohammad Kazem Fallahzadeh, Payaswini Vasanth, Christian Larsen\",\"doi\":\"10.1111/tid.14298\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The effect of belatacept on BK polyomavirus (BKPyV) control remains largely unknown.</p><p><strong>Methods: </strong>This is a propensity matched retrospective cohort study in adult kidney transplant recipients (KTR) transplanted between 2016-2020 who received a belatacept- versus tacrolimus-based immunosuppression regimen. A continuous time multi-state Markov model was used to evaluate BKPyV replication dynamics (BKPyV-dyn). Three BKPyV-dyn states were defined: BKPyV-dyn1 (viral load <3 log<sub>10</sub>), BKPyV-dyn2 (viral load ≥ 3 log<sub>10</sub> and ≤4 log<sub>10</sub>), and BKPyV-dyn3 (viral load >4 log<sub>10</sub>).</p><p><strong>Results: </strong>Two hundred eighty KTR on belatacept- and 280 KTR on tacrolimus-based regimens were compared. The probability of transitioning between BKPyV-dyn states and time spent in each state in both groups was comparable. Total duration in BKPyV-dyn-1 was 632.1 days (95% CI 612.1, 648.5) for belatacept versus 615.2 days (95% CI 592.5, 635.8) for tacrolimus, BKPyV-dyn-2 was 49.2 days (95% CI 41.3, 58.4) for belatacept versus 55.6 days (95% CI 46.5, 66.8) for tacrolimus, and BKPyV-dyn-3 was 48.7 days (95% CI 37.1, 363.1) for belatacept versus 59.2 days (95% CI 45.8, 73.5) for tacrolimus. 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引用次数: 0
摘要
背景：贝拉他赛普对 BK 多瘤病毒（BKPyV）的控制效果仍是未知数：贝拉替塞对BK多瘤病毒（BKPyV）控制的影响在很大程度上仍然未知：这是一项倾向匹配的回顾性队列研究，研究对象是2016-2020年间接受贝拉替塞与他克莫司免疫抑制方案的成人肾移植受者（KTR）。研究采用连续时间多状态马尔可夫模型来评估 BKPyV 复制动态（BKPyV-dyn）。该模型定义了三种 BKPyV-dyn 状态：BKPyV-dyn1（病毒载量为 10）、BKPyV-dyn2（病毒载量≥3 log10 且≤4 log10）和 BKPyV-dyn3（病毒载量>4 log10）：比较了280名KTR使用贝拉替塞疗法和280名KTR使用他克莫司疗法的情况。两组患者在 BKPyV-dyn 状态之间转换的概率以及在每种状态下停留的时间相当。贝拉坦普治疗 BKPyV-dyn-1 的总持续时间为 632.1 天（95% CI 612.1，648.5），而他克莫司治疗 BKPyV-dyn-2 的总持续时间为 615.2 天（95% CI 592.5，635.8）；贝拉坦普治疗 BKPyV-dyn-2 的总持续时间为 49.2 天（95% CI 41.3，58.BKPyV-dyn-2为49.2天（95% CI 41.3，58.4），贝拉替塞为55.6天（95% CI 46.5，66.8），他克莫司为55.6天（95% CI 46.5，66.8）；BKPyV-dyn-3为48.7天（95% CI 37.1，363.1），贝拉替塞为59.2天（95% CI 45.8，73.5），他克莫司为59.2天（95% CI 45.8，73.5）。BKPyV相关肾病（PyVAN）在贝拉替塞普治疗的KRT中发生率为3.9%，在他克莫司治疗的KRT中发生率为3.9%（P > .9）：结论：与他克莫司免疫抑制相比，贝拉他赛普免疫抑制不会增加BKPyV-DNA血症或肾病的风险。
Belatacept-based immunosuppression does not confer increased risk of BK polyomavirus-DNAemia relative to tacrolimus-based immunosuppression.
Background: The effect of belatacept on BK polyomavirus (BKPyV) control remains largely unknown.
Methods: This is a propensity matched retrospective cohort study in adult kidney transplant recipients (KTR) transplanted between 2016-2020 who received a belatacept- versus tacrolimus-based immunosuppression regimen. A continuous time multi-state Markov model was used to evaluate BKPyV replication dynamics (BKPyV-dyn). Three BKPyV-dyn states were defined: BKPyV-dyn1 (viral load <3 log10), BKPyV-dyn2 (viral load ≥ 3 log10 and ≤4 log10), and BKPyV-dyn3 (viral load >4 log10).
Results: Two hundred eighty KTR on belatacept- and 280 KTR on tacrolimus-based regimens were compared. The probability of transitioning between BKPyV-dyn states and time spent in each state in both groups was comparable. Total duration in BKPyV-dyn-1 was 632.1 days (95% CI 612.1, 648.5) for belatacept versus 615.2 days (95% CI 592.5, 635.8) for tacrolimus, BKPyV-dyn-2 was 49.2 days (95% CI 41.3, 58.4) for belatacept versus 55.6 days (95% CI 46.5, 66.8) for tacrolimus, and BKPyV-dyn-3 was 48.7 days (95% CI 37.1, 363.1) for belatacept versus 59.2 days (95% CI 45.8, 73.5) for tacrolimus. BKPyV associated nephropathy (PyVAN) occurred in 3.9% in belatacept- and 3.9% tacrolimus-treated KRT (P > .9).
Conclusions: Compared with tacrolimus-based immunosuppression, belatacept based immunosuppression was not associated with increased risk of BKPyV-DNAemia or nephropathy.
期刊介绍：
Transplant Infectious Disease has been established as a forum for presenting the most current information on the prevention and treatment of infection complicating organ and bone marrow transplantation. The point of view of the journal is that infection and allograft rejection (or graft-versus-host disease) are closely intertwined, and that advances in one area will have immediate consequences on the other. The interaction of the transplant recipient with potential microbial invaders, the impact of immunosuppressive strategies on this interaction, and the effects of cytokines, growth factors, and chemokines liberated during the course of infections, rejection, or graft-versus-host disease are central to the interests and mission of this journal.
Transplant Infectious Disease is aimed at disseminating the latest information relevant to the infectious disease complications of transplantation to clinicians and scientists involved in bone marrow, kidney, liver, heart, lung, intestinal, and pancreatic transplantation. The infectious disease consequences and concerns regarding innovative transplant strategies, from novel immunosuppressive agents to xenotransplantation, are very much a concern of this journal. In addition, this journal feels a particular responsibility to inform primary care practitioners in the community, who increasingly are sharing the responsibility for the care of these patients, of the special considerations regarding the prevention and treatment of infection in transplant recipients. As exemplified by the international editorial board, articles are sought throughout the world that address both general issues and those of a more restricted geographic import.
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