| Literature DB >> 32741096 |
Ilies Benotmane1,2,3, Morgane Solis2,3, Aurélie Velay2,3, Noëlle Cognard1,3, Jérôme Olagne1,3,4, Gabriela Gautier Vargas1,3, Peggy Perrin1,3, David Marx1,3, Eric Soulier3, Floriane Gallais2,3, Bruno Moulin1,3, Samira Fafi-Kremer2,3, Sophie Caillard1,3.
Abstract
BK virus (BKV) replication occurs frequently in kidney transplant recipients (KTR), potentially leading to BKV-associated nephropathy (BKVAN) and graft loss. Patients with high titers of BKV-neutralizing antibodies (NAbs) are protected against BKV replication, and intravenous immunoglobulin (IVIg) infusion can increase NAb titers. We investigated whether early IVIg administration prevents BKV replication in patients with low NAb titers (<4 log10 against the BKV-specific genotype). Based on NAb titers on the day of transplantation, KTR followed in the Strasbourg University Hospital (n = 174) were retrospectively divided into the following 3 risk categories for BKV replication: (1) patients with low NAb titers ("high-risk") who received IVIg for the first 3 posttransplant months (n = 44), (2) patients with low NAb titers ("high-risk") who did not undergo IVIg treatment (n = 41), and (3) patients with high NAb titers ("low-risk") who did not receive IVIg (n = 89). At 12 posttransplant months, the incidence of BKV viremia in the high-risk group treated with IVIg (6.8%) was similar to that observed in the low-risk group (10.1%) and markedly lower than that of the untreated high-risk group (36.6%; P < .001). Similar results were observed with regard to BKVAN. We conclude that IVIg may be a valuable strategy for preventing BKV replication.Entities:
Keywords: antibiotic: antiviral; clinical research/practice; complication: infectious; infection and infectious agents - viral: BK/JC/polyoma; infectious disease; kidney transplantation/nephrology
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Year: 2020 PMID: 32741096 DOI: 10.1111/ajt.16233
Source DB: PubMed Journal: Am J Transplant ISSN: 1600-6135 Impact factor: 8.086