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Case Reports in Transplantation
Volume 2017 (2017), Article ID 3624146, 7 pages
https://doi.org/10.1155/2017/3624146
Case Report

Brincidofovir Use after Foscarnet Crystal Nephropathy in a Kidney Transplant Recipient with Multiresistant Cytomegalovirus Infection

1Centre de Néphrologie et Transplantation Rénale, Hôpital Conception, Assistance Publique-Hôpitaux de Marseille, Marseille, France
2Aix-Marseille University, Marseille, France
3Fédération de Bactériologie-Virologie-Hygiène, Hôpital Timone, Assistance Publique-Hôpitaux de Marseille, Marseille, France
4Laboratoire de Bactériologie-Virologie-Hygiène, Centre Hospitalier Universitaire, Limoges, France
5Pharmacie Hospitalière, Hôpital Conception, Assistance Publique-Hôpitaux de Marseille, Marseille, France
6Laboratoire d’Anatomie Pathologique, Hôpital Timone, Assistance Publique-Hôpitaux de Marseille, Marseille, France

Correspondence should be addressed to Tristan Legris; rf.mh-pa@sirgel.natsirt

Received 26 December 2016; Accepted 12 February 2017; Published 27 February 2017

Academic Editor: Frieder Keller

Copyright © 2017 Romain Vial et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Cytomegalovirus (CMV) antiviral drug resistance constitutes an increasing challenge in transplantation. Foscarnet is usually proposed when resistance for ganciclovir is suspected, but its use is limited by its nephrotoxicity. Case Presentation. We report a case of multiresistant CMV disease in a kidney transplant recipient. Foscarnet was prescribed after ganciclovir treatment failure in a patient with two mutations in the UL97 viral gene. Foscarnet induced biopsy-proven kidney crystal precipitation that resulted in severe acute transplant failure and nephrotic syndrome. Despite a large decrease in immunosuppression, CMV disease was not controlled and a salvage therapy with Brincidofovir (BCV), which is an oral lipid conjugate of cidofovir with limited nephrotoxicity, was attempted. Clinical and virological remission was observed after a 21-day course of BCV, despite mild and reversible liver toxicity. However, a new relapse could not be effectively cured by BCV due to a new mutation in the UL54 gene, which is known to confer resistance to cidofovir. A new course of foscarnet finally resulted in prolonged CMV remission. Herein, we present a review of foscarnet nephropathy cases in solid-organ transplanted patients. Conclusions. This unique case highlights the potential benefit of BCV use during resistant CMV infection, although mutations in the UL54 gene may limit its therapeutic efficacy. These findings need to be confirmed in clinical trials.