[Nephrotoxicity of anti-angiogenesis drugs]

Area of Science:

• Oncology
• Nephrology
• Molecular Biology

Background:

• Neoangiogenesis, driven by vascular endothelium growth factor (VEGF) and its receptors (VEGFR1/2), is crucial for physiological and pathological processes like tumor metastasis.
• Antiangiogenic agents targeting VEGF (e.g., bevacizumab) or VEGFR2 (e.g., ramucirumab) are integral to modern cancer chemotherapy.
• The VEGF-VEGFR signaling pathway is vital for maintaining normal kidney function.

Purpose of the Study:

• To review the mechanisms, clinical presentations, and morphological characteristics of nephropathy induced by antiangiogenic drugs.
• To elucidate the adverse renal effects associated with VEGF-targeted therapies in oncology.

Main Methods:

• Literature review of studies on antiangiogenic agents and their impact on renal function.
• Analysis of clinical and histopathological data concerning drug-induced nephrotoxicity.

Main Results:

• Antiangiogenic therapies can lead to significant adverse nephrotoxic effects, including hypertension, proteinuria, and kidney dysfunction.
• Thrombotic microangiopathy of renal vessels is a common histopathological finding in drug-associated nephropathy.
• Various histological variants of nephropathy have been described in patients treated with these agents.

Conclusions:

• Antiangiogenic drugs, while effective in cancer treatment, pose a risk of significant renal toxicity.
• Understanding the mechanisms and clinical manifestations of antiangiogenic drug-induced nephropathy is essential for patient management.
• Further research is needed to mitigate or prevent these adverse renal effects in cancer patients.