De novo thrombotic microangiopathy in two kidney transplant recipients from the same deceased donor: A case series.
complement biology
ischemia reperfusion injury (IRI)
kidney (allograft) function/dysfunction
organ procurement
outpatient care
Journal
Clinical transplantation
ISSN: 1399-0012
Titre abrégé: Clin Transplant
Pays: Denmark
ID NLM: 8710240
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
18
02
2020
revised:
09
04
2020
accepted:
13
04
2020
pubmed:
22
4
2020
medline:
11
6
2021
entrez:
22
4
2020
Statut:
ppublish
Résumé
Thrombotic microangiopathy (TMA) is a recognized and serious complication of renal transplantation. Atypical hemolytic uremic syndrome (aHUS), a subset of TMA, occurs in the setting of dysregulation of the alternative complement pathway and can cause disease in native kidneys as well as recurrence in allografts. De novo TMA represents a classification of TMA post-transplant in the absence of clinical or histopathological evidence of TMA or aHUS in the native kidney. De novo TMA is a more heterogeneous syndrome than aHUS and the pathogenesis and risk factors for de novo TMA are poorly understood. The association between calcineurin inhibitors (CNI) and de novo TMA is controversial. Anti-complement blockade therapy with eculizumab is effective in some cases, but more studies are needed to identify appropriate candidates for therapy. We present two cases of de novo TMA occurring immediately in recipients from the same deceased donor and provoking the question of whether deceased donor-related factors could represent risks for developing de novo TMA.
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13885Informations de copyright
© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
Références
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