Renal toxicity during VEGF-pathway inhibition in cancer: a practical review of proteinuria, hypertension, and kidney-limited thrombotic microangiopathy

Vascular endothelial growth factor (VEGF)-pathway inhibitors improve outcomes across solid tumors, but proteinuria, hypertension and kidney dysfunction can be difficult to translate into oncology decisions. Most abnormalities are manageable on-target toxicities; a smaller subset may signal glomerular microvascular injury or kidney-limited thrombotic microangiopathy, sometimes without overt hemolysis or thrombocytopenia. This narrative review synthesizes mechanistic, clinical, pharmacovigilance and biopsy-based evidence to support an oncology-facing approach to renal toxicity during VEGF/VEGF receptor (VEGFR) inhibition. We emphasize baseline renal assessment, longitudinal interpretation of proteinuria and blood pressure, exclusion of competing causes, earlier nephrology input when findings are progressive or treatment-relevant, and selective biopsy when histology may change continuation, dose reduction, interruption, switching or rechallenge. The framework is pragmatic and hypothesis-generating rather than guideline-level or prospectively validated, aiming to preserve effective anticancer therapy while avoiding delayed recognition of clinically meaningful glomerular injury.