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Anti-VEGF Vascular Toxicity — SCE Medical Oncology MCQ

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ModerateImmunotherapy & Targeted TherapyAnti-VEGF Vascular ToxicitySCE Medical Oncology

A 65-year-old man on a multi-kinase inhibitor for HCC develops proteinuria (2 g/24 hours) and hypertension (BP 160/95). These are class effects of anti-VEGF agents. What is the underlying vascular mechanism?

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Correct answer: B — Inhibition of VEGF signalling in glomerular endothelium reduces nitric oxide production, causing endothelial dysfunction, hypertension and proteinuria (thrombotic microangiopathy spectrum)

Anti-VEGF agents (bevacizumab, VEGFR-TKIs) cause hypertension and proteinuria through a shared mechanism: VEGF is essential for maintaining glomerular endothelial fenestrations and nitric oxide production. VEGF inhibition causes loss of fenestrations, decreased NO, vasoconstriction, and glomerular endotheliosis (resembling pre-eclampsia or thrombotic microangiopathy). This explains why all anti-VEGF therapies share these renal/cardiovascular toxicities as class effects.

Reference: ESMO 2024 Cardio-Oncology/Supportive Care Guidelines; Izzedine et al NEJM 2008