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Use of Eculizumab in Transplant-Associated Thrombotic Microangiopathy in a Patient With Polycystic Kidney Disease Immediately Post–Kidney Transplant: A Case Report

Transplant-associated thrombotic microangiopathy (TMA) in the post–organ transplantation setting occurs from a number of potential inciting factors, such as the use of calcineurin inhibitors, ischemic injury, infections, or antibody-mediated rejection leading to unchecked complement activation and e...

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Detalles Bibliográficos
Autores principales: Godara, Amandeep, Migliozzi, Daniel R., Pilichowska, Monika, Goyal, Nitender, Varga, Cindy, Gordon, Craig E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568057/
https://www.ncbi.nlm.nih.gov/pubmed/33089142
http://dx.doi.org/10.1016/j.xkme.2020.06.007
Descripción
Sumario:Transplant-associated thrombotic microangiopathy (TMA) in the post–organ transplantation setting occurs from a number of potential inciting factors, such as the use of calcineurin inhibitors, ischemic injury, infections, or antibody-mediated rejection leading to unchecked complement activation and end-organ damage. Delayed recognition of this condition can result in allograft loss. In this case description, we describe the first case of de novo TMA in a patient with polycystic kidney disease that occurred immediately after kidney transplantation. The diagnosis was made promptly on the basis of clinical and laboratory characteristics by a multidisciplinary team and confirmed through kidney biopsy, which showed acute TMA. The patient was successfully managed by replacing tacrolimus with belatacept, which targets cytotoxic T lymphocyte antigen 4, and use of eculizumab, a C5 inhibitor. Eculizumab treatment was discontinued after 3 months of complement inhibition on the patient’s request, and relapse of TMA has not been encountered after more than 1 year of follow-up.