Key result
Antiangiogenic therapies share class-effect proteinuria and hypertension driven by VEGF pathway inhibition.
Why the study?
Do antiangiogenic therapies cause hypertension and proteinuria as a class effect in patients with solid tumor cancers?
Do antiangiogenic therapies cause hypertension and proteinuria as a class effect in patients with solid tumor cancers?
Hypertension and proteinuria are class effects of all antiangiogenic therapies, requiring appropriate monitoring and management by clinicians.
Supports monitoring for proteinuria and hypertension with antiangiogenic agents; leaves open prospective validation of uniform VEGF class effects.
Antiangiogenic therapy has now become a cornerstone in the treatment of several solid tumor cancers. Those drugs present with a renal toxicity profile manifesting as proteinuria and hypertension, often reported in the literature to be linked to bevacizumab, a monoclonal antibody targeted at the circulating vascular endothelial growth factor (VEGF). However, there is evidence that those side effects are most probably related to the pharmacological action of those drugs: the inhibition of the VEGF pathway. Thus, they may occur with any antiangiogenic therapy, either those acting on circulating VEGF (bevacizumab or VEGF-trap), or those acting on VEGF receptor(s) (sunitinib, sorafenib, or axitinib). Clinicians should thus be aware of such a 'class effect' to appropriately monitor and treat their patients, regardless of which antiangiogenic drug is used.
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Launay‐Vacher et al. (2008) conducted a review in Solid tumor cancers. Antiangiogenic therapies was evaluated on Proteinuria and hypertension. Antiangiogenic therapies share a class-effect renal toxicity profile manifesting as proteinuria and hypertension due to the inhibition of the VEGF pathway.
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