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

Created on 07 Jul 2026

Authors

Lucas Maciel de Almeida Corrêa, Ana Laura Mendes Lourenço, Luiggi Kevin Virgino Brandão, Gabriel Rian Mazur, Alexandre de Assis Barbosa, Clara Belo Gamon Santiago, Ivan Felipe Dutra Júnior, Rodrigo Galetto Husch, Yan Roberth Delmiro Silva, Gabriel Costa de Santana, Letícia Esteves Dante

Published in

Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico. Jul 06, 2026. Epub Jul 06, 2026.

Abstract

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.

PMID:
42410275
Bibliographic data and abstract were imported from PubMed on 07 Jul 2026.

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