VEGF Inhibition and Renal Thrombotic Microangiopathy

In six patients who received bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), proteinuria subsequently developed, and thrombotic microangiopathy was shown on renal biopsy. In a murine model, the authors showed that using conditional gene targeting to ablate the VEGF gene from renal podocytes can trigger thrombotic microangiopathy. This finding suggests that glomerular injury from bevacizumab may be due to the direct targeting of VEGF. In six patients who received bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), proteinuria subsequently developed and thrombotic microangiopathy was shown on renal biopsy. Findings from this study suggest that glomerular injury from bevacizumab may be due to the direct targeting of VEGF. The discovery that vascular endothelial growth factor (VEGF) is a critical factor in the growth of blood vessels led to the development of VEGF inhibitors, such as bevacizumab, to treat diseases that are characterized by pathologic angiogenesis. The addition of bevacizumab to chemotherapeutic regimens improved survival rates among patients with cancers of the colon, lung, and breast; it is also used as a single agent for renal-cell carcinoma. With the expanding use of bevacizumab, adverse effects have become apparent. Two of the most common are proteinuria (in 21 to 64% of patients) and hypertension (in 3 to 36%). 1 Nephrotic-range proteinuria, . . .