TY - JOUR
T1 - De novo thrombotic microangiopathy immediately after kidney transplant in patients without apparent risk factors
AU - Patel, Ankita
AU - Knorr, John P.
AU - Campos, Stalin
AU - Khanmoradi, Kamran
AU - Zaki, Radi F.
AU - Bradauskaite, Gitana
N1 - Publisher Copyright:
© Baskent University 2016 Printed in Turkey. All Rights Reserved.
PY - 2016/4
Y1 - 2016/4
N2 - Thrombotic microangiopathy refers to a spectrum of conditions that share a common underlying pathologic mechanism that result in endothelial damage and microangiopathic hemolytic anemia. De novo thrombotic microangiopathy after kidney transplant is often triggered by immunosuppressive drugs, and studies most often implicate calcineurin inhibitors and/or mammalian target of rapamycin inhibitors; however, muromonab and alemtuzumab also reportedly cause thrombotic microangiopathy. In addition, thrombotic microangiopathy may be triggered by acute antibody-mediated rejection and infections like cytomegalovirus and parvovirus. Here, we present a case series of 3 patients without any apparent risk factors (eg, acute antibody-mediated rejection) who developed de novo thrombotic microangiopathy immediately following kidney transplant, but before the introduction of calcineurin inhibitors. Two of these 3 patients were successfully managed with plasma exchange, and calcineurin inhibitors were successfully introduced without the recurrence of thrombotic microangiopathy.
AB - Thrombotic microangiopathy refers to a spectrum of conditions that share a common underlying pathologic mechanism that result in endothelial damage and microangiopathic hemolytic anemia. De novo thrombotic microangiopathy after kidney transplant is often triggered by immunosuppressive drugs, and studies most often implicate calcineurin inhibitors and/or mammalian target of rapamycin inhibitors; however, muromonab and alemtuzumab also reportedly cause thrombotic microangiopathy. In addition, thrombotic microangiopathy may be triggered by acute antibody-mediated rejection and infections like cytomegalovirus and parvovirus. Here, we present a case series of 3 patients without any apparent risk factors (eg, acute antibody-mediated rejection) who developed de novo thrombotic microangiopathy immediately following kidney transplant, but before the introduction of calcineurin inhibitors. Two of these 3 patients were successfully managed with plasma exchange, and calcineurin inhibitors were successfully introduced without the recurrence of thrombotic microangiopathy.
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U2 - 10.6002/ect.2014.0089
DO - 10.6002/ect.2014.0089
M3 - Article
C2 - 26030297
AN - SCOPUS:84962642564
SN - 1304-0855
VL - 14
SP - 230
EP - 234
JO - Experimental and Clinical Transplantation
JF - Experimental and Clinical Transplantation
IS - 2
ER -