Renal-limited thrombotic microangiopathy after switching from bevacizumab to ramucirumab: a case report

Abstract Background It is well known that vascular endothelial growth factor (VEGF) inhibitors can cause proteinuria. The incidence of proteinuria is high for bevacizumab, a humanized monoclonal antibody directed against VEGF, but the range of proteinuria rarely becomes nephrotic (2.2% occurrence ac...

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Bibliographic Details
Main Authors: Ryo Yamada, Takao Okawa, Ken Matsuo, Makoto Suzuki, Noriko Mori, Kiyoshi Mori
Format: Article
Language:English
Published: BMC 2019-01-01
Series:BMC Nephrology
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12882-018-1194-9
Description
Summary:Abstract Background It is well known that vascular endothelial growth factor (VEGF) inhibitors can cause proteinuria. The incidence of proteinuria is high for bevacizumab, a humanized monoclonal antibody directed against VEGF, but the range of proteinuria rarely becomes nephrotic (2.2% occurrence according to a meta-analysis). In such cases, renal pathology shows thrombotic microangiopathy (TMA). Ramucirumab, anti-VEGF receptor 2 (VEGFR2) monoclonal antibody, can also cause proteinuria, but it is not yet reported whether the drug may induce TMA. Case presentation Here, we report a case who immediately developed TMA by ramucirumab after multiple courses of bevacizumab treatment. This is the first case of pathologically-proved TMA by ramucirumab. After cessation of the drug, symptoms of TMA improved gradually. Conclusions This case demonstrates that not only blockade of VEGF but also VEGFR2 antagonism may result in TMA, which is a rare but life-threatening complication of cancer treatment drug.
ISSN:1471-2369