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Thrombotic Microangiopathy after Lung Transplantation
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Background.
Thrombotic microangiopathy (TMA) is a well-recognized complication after transplantation. The purpose of this study was to describe our center’s experience with this complication after lung transplantation.
Methods.
We retrospectively reviewed cases of TMA among patients who underwent lung transplantation between January 1, 1999 and December 31, 2003 (n=257). The cases were characterized and the outcomes were analyzed. Univariate and multivariate Cox regression models were constructed to identify potential risk factors for TMA.
Results.
Twenty-four cases of TMA developed in 20 recipients. Thirteen cases occurred in the setting of another illness and 11 cases were isolated complications. Multivariate Cox regression models identified female gender, history of TMA, and the immunosuppressive regimen as independent predictors of TMA. Maintenance immunosuppression with the combination of a calcineurin inhibitor and sirolimus carried a significantly higher risk of TMA than a calcineurin inhibitor alone. After the diagnosis of TMA, calcineurin inhibitors were stopped in 18 cases; however, in 6 cases in which the onset of TMA coincided with the addition of sirolimus to a calcineurin inhibitor, only sirolimus was discontinued. Plasmapheresis was performed for severe cases (n=10). TMA remitted in all cases, and an alternate calcineurin inhibitor was introduced in 14 cases. TMA recurred in 4 recipients, a median 253 days after the initial episode. The median survival after the onset of TMA was 377 days.
Conclusion.
TMA is a serious complication after lung transplantation, and the risk is highest when sirolimus is used in combination with a calcineurin inhibitor.
Ovid Technologies (Wolters Kluwer Health)
Title: Thrombotic Microangiopathy after Lung Transplantation
Description:
Background.
Thrombotic microangiopathy (TMA) is a well-recognized complication after transplantation.
The purpose of this study was to describe our center’s experience with this complication after lung transplantation.
Methods.
We retrospectively reviewed cases of TMA among patients who underwent lung transplantation between January 1, 1999 and December 31, 2003 (n=257).
The cases were characterized and the outcomes were analyzed.
Univariate and multivariate Cox regression models were constructed to identify potential risk factors for TMA.
Results.
Twenty-four cases of TMA developed in 20 recipients.
Thirteen cases occurred in the setting of another illness and 11 cases were isolated complications.
Multivariate Cox regression models identified female gender, history of TMA, and the immunosuppressive regimen as independent predictors of TMA.
Maintenance immunosuppression with the combination of a calcineurin inhibitor and sirolimus carried a significantly higher risk of TMA than a calcineurin inhibitor alone.
After the diagnosis of TMA, calcineurin inhibitors were stopped in 18 cases; however, in 6 cases in which the onset of TMA coincided with the addition of sirolimus to a calcineurin inhibitor, only sirolimus was discontinued.
Plasmapheresis was performed for severe cases (n=10).
TMA remitted in all cases, and an alternate calcineurin inhibitor was introduced in 14 cases.
TMA recurred in 4 recipients, a median 253 days after the initial episode.
The median survival after the onset of TMA was 377 days.
Conclusion.
TMA is a serious complication after lung transplantation, and the risk is highest when sirolimus is used in combination with a calcineurin inhibitor.
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