Scholarlink

<p>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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月6日

查看全文
  • 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

摘要

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.