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Published on: September 1, 2016
Renal effects of anti-angiogenesis therapy: update for the internist
Faina Gurevich1, Mark A Perazella
1Department of Medicine, Yale University School of Medicine, New Haven, CT 06520-8029, USA.
Abstract:
Angiogenesis has become an innovative target in cancer therapy. Agents that inhibit vascular endothelial growth factor (VEGF), one of the most potent promoters of angiogenesis, and its receptor have significant implications for clinical practice. Bevacizumab, sorafenib, sunitinib and other anti-VEGF drugs are frequently complicated by mild proteinuria and hypertension. Other unique renal effects, such as high-grade proteinuria and acute kidney injury, have been described. The most common histopathologic kidney lesion is thrombotic microangiopathy, with other glomerular lesions and interstitial nephritis occurring less frequently. The mechanism for anti-VEGF therapy-induced hypertension is not well understood; however, nitric oxide pathway inhibition, rarefaction, and oxidative stress may be important in its pathogenesis. Glomerular injury may develop from loss of VEGF effect on maintaining the filtration barrier. Adverse effects of anti-VEGF class of drugs are manageable but require close attention and follow-up. Understanding the fundamentals of anti-VEGF drugs' mechanism of action and their clinical implications is crucial when caring for patients receiving anti-VEGF therapy.
Insights
Anti-vascular endothelial growth factor (VEGF) cancer therapies can cause kidney problems like proteinuria and acute kidney injury. Close monitoring is essential for managing these adverse effects in patients undergoing anti-VEGF treatment.
Area of Science:
- Oncology
- Nephrology
- Pharmacology
Background:
- Angiogenesis is a key target in cancer therapy.
- Vascular Endothelial Growth Factor (VEGF) inhibitors are widely used in cancer treatment.
- These drugs can cause significant renal side effects.
Purpose of the Study:
- To review the renal effects of anti-VEGF therapies.
- To discuss the mechanisms behind these adverse events.
- To emphasize the importance of monitoring patients on anti-VEGF drugs.
Main Methods:
- Literature review of studies on anti-VEGF drugs and renal effects.
- Analysis of histopathological findings in affected patients.
- Discussion of proposed pathogenetic mechanisms for hypertension and glomerular injury.
Main Results:
- Common side effects include mild proteinuria and hypertension.
- High-grade proteinuria and acute kidney injury can occur.
- Thrombotic microangiopathy is the most frequent kidney lesion observed.
- Other lesions include glomerular injury and interstitial nephritis.
Conclusions:
- Anti-VEGF therapies present unique renal challenges.
- Mechanisms involve nitric oxide pathway inhibition, rarefaction, and oxidative stress.
- Glomerular injury may stem from impaired filtration barrier maintenance.
- Adverse effects are manageable with careful patient management and follow-up.
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