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NDT Plus Advance Access originally published online on March 11, 2008
NDT Plus 2008 1(3):154-156; doi:10.1093/ndtplus/sfn013
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Thrombotic microangiopathy associated with sunitinib, a VEGF inhibitor, in a patient with factor V Leiden mutation

Seth A. Levey1, Randeep S. Bajwa1, Maria M. Picken2, Joseph I. Clark1, Kevin Barton1 and David J. Leehey1

1 Department of Medicine
2 Department of Pathology, Loyola University Medical Center, Maywood, IL 60153, USA and Veterans Affairs Hospital, Hines, IL 60141, USA

Correspondence: David J. Leehey, Loyola University Medical Center, Bldg 102, Rm. 3661, 2160 S., 1st Avenue, Maywood, IL 60153, USA. Tel: +1-708-2163-306; Fax: +1-708-2164-060; E-mail: dleehey@lumc.edu

Key Words: Factor V Leiden • sunitinib • thrombotic microangiopathy • VEGF inhibitors

Received for publication October 28, 2007. Accepted for publication January 23, 2008.

The first 10% of the full text of this article appears below.

Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are closely related disorders characterised by non-immune microangiopathic haemolytic anaemia and thrombocytopenia. Thrombotic microangiopathy is the underlying pathologic lesion in both syndromes. Under physiological conditions, platelets bind to endothelium via von Willebrand Factor (vWF) and are released back into the circulation by ADAMTS13, a metalloprotease that cleaves ultra-large, newly synthesized vWF multimers. A deficiency of ADAMTS13 (due to either a decrease in its production or the presence of a circulating inhibitor) may thus result in microvascular thrombi. However, patients with thrombotic microangiopathy may have normal ADAMTS13 levels and no evidence of a circulating inhibitor [1].

Sunitinib malate, an oral . . . [Full Text of this Article]


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