Thrombotic microangiopathy (TMA) is a complication that can develop directly from certain malignancies, but more often results from anticancer therapy. Currently, the incidence of cancer drug-induced TMA during the last few decades is >15%, primarily due to the introduction of anti-vascular endothelial growth factor (VEGF) agents. It is important for clinicians to understand the potential causes of cancer drug-induced TMA to facilitate successful diagnosis and treatment. In general, cancer drug-induced TMA can be classified into 2 types. Type I cancer drug-induced TMA includes chemotherapy regimens (ie, mitomycin C) that can potentially promote long-term kidney injury, as well as increased morbidity and mortality. Type II cancer drug-induced TMA includes anti-VEGF agents that are not typically associated with cumulative dose-dependent cell damage. In addition, functional recovery of kidney function often occurs after drug interruption, assuming a type I agent was not given prior to or during therapy. There are no randomized controlled trials to provide physician guidance in the management of TMA. However, previously accumulated information and research suggest that endothelial cell damage has an underlying immunologic basis. Based on this, the emerging trend includes the use of immunosuppressive agents if a refractory or relapsing clinical course that does not respond to plasmapheresis and steroids is observed.
Keywords: ACDIT; DIC; Thrombotic microangiopathy; anti-VEGF; chemotherapy; disseminated intravascular coagulopathy; drug-induced TMA; onco-nephrology; review.
Copyright © 2015 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.