Why the study?
The emergence of antiangiogenic agents has led to adverse nephrotoxic effects, including arterial hypertension, proteinuria, nephrotic syndrome, and kidney dysfunction.
What are the mechanisms and clinical aspects of nephropathy associated with antiangiogenic drugs?
What are the mechanisms and clinical aspects of nephropathy associated with antiangiogenic drugs?
Answers are grounded in this paper and cite their sources.
Antiangiogenic drugs used in oncology can cause significant nephrotoxicity, primarily manifesting as arterial hypertension, proteinuria, and thrombotic microangiopathy.
Neoangiogenesis is a basic factor for most physiological as well as pathological processes i.e. tumor metastases. The most important is vascular endothelium growth factor (VEGF) and its receptors (VEGFR1/2) in angiogenesis processes. Nowadays antiangiogenic agents (which inhibit VEGF like bevacizumab neither VEGFR2 like ramucirumab) are widely used in very different chemotherapeutic regimens in clinical oncology. The signalling pathway VEGF-VEGFR plays a crucial role in supporting of adequate kidney function. Appearance of antiangiogenic drugs led to adverse nephrotoxic effects: arterial hypertension, proteinuria, rarely nephrotic syndrome, and kidney dysfunction. Various hystological variants of nephropathy are described, however, in most cases, signs of thrombotic microangiopathy of the renal vessels are noted. This literature review discusses mechanisms, clinical and morphological aspects of nephropathy associated with antiangiogenic drugs.
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Grechukhina et al. (2020) conducted a review in Nephrotoxicity induced by antiangiogenic antitumor drugs. Anti-angiogenesis drugs (bevacizumab, aflibercept, ramucirumab) was evaluated.
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