Abstract
BackgroundIt 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 presentationHere, 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.ConclusionsThis 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.
Highlights
It is well known that vascular endothelial growth factor (VEGF) inhibitors can cause proteinuria
This case demonstrates that blockade of VEGF and VEGF receptor 2 (VEGFR2) antagonism may result in thrombotic microangiopathy (TMA), which is a rare but life-threatening complication of cancer treatment drug
Vascular endothelial growth factor (VEGF) inhibitors are increasingly applied to treat a number of malignancies such as metastatic or recurrent colorectal, non-small cell lung, breast, and renal cell cancers
Summary
This case demonstrates that blockade of VEGF and VEGFR2 antagonism may result in TMA, which is a rare but life-threatening complication of cancer treatment drug.
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