Belatacept as Maintenance Immunosuppression for Postrenal Transplant de novo Drug‐Induced Thrombotic Microangiopathy
De novo posttransplant thrombotic microangiopathy (TMA) is a complication of solid organ transplantation, which remains difficult to treat. In many cases, immunosuppressants and particularly calcineurin inhibitors, trigger TMA. Although withdrawing the offending drug may lead to resolution of TMA, g...
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Published in: | American journal of transplantation Vol. 9; no. 2; pp. 424 - 427 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Malden, USA
Blackwell Publishing Inc
01-02-2009
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Subjects: | |
Online Access: | Get full text |
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Summary: | De novo posttransplant thrombotic microangiopathy (TMA) is a complication of solid organ transplantation, which remains difficult to treat. In many cases, immunosuppressants and particularly calcineurin inhibitors, trigger TMA. Although withdrawing the offending drug may lead to resolution of TMA, graft and patient outcomes are poor. Specific treatments, including plasma exchange, have not gained widespread acceptance in those with fulminant disease and new approaches to the condition are urgently needed.
We report a case of posttransplant de novo TMA presenting serially in association with ciclosporin, tacrolimus and sirolimus in a young recipient of a living donor kidney transplant. We describe a patient treated with belatacept, a novel CTLA4 Ig fusion protein, as ongoing maintenance immunosuppression to allow avoidance of conventional agents once associated with TMA. We report excellent early graft outcome, with no adverse events using this strategy. We suggest that belatacept may have a role in this traditionally difficult‐to‐treat group of patients.
A young living donor recipient achieved excellent graft function without rejection on monthly belatacept infusions after repeated episodes of thrombotic microangiopathy on cyclosporine, tacrolimus and sirolimus. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1600-6135 1600-6143 |
DOI: | 10.1111/j.1600-6143.2008.02482.x |