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Tumoral angiogenesis is a key mechanism in the growth and spread of cancer cells. The development of angiogenesis inhibitors, particularly those targeting the vascular endothelial growth factor (VEGF) pathway, has improved the prognosis and survival of many cancer patients since these drugs were first approved in France in 2005. Angiogenesis inhibitors have various mechanisms of action, targeting either the ligand (as with the anti-VEGF monoclonal antibody bevacizumab, and the anti-VEGF recombinant fusion protein aflibercept), or its receptors, as with tyrosine kinase inhibitors (such as sunitinib or sorafenib). These treatments can be combined with conventional chemotherapy or other anti-cancer therapies, and are associated with variable tolerability depending on the patient’s clinical condition and comorbidities. Angiogenesis inhibitors can also be associated with cardiovascular toxicity and/or nephrotoxicity, and special monitoring is therefore needed for the duration of treatment. Hypertension and proteinuria are the most common renal adverse effects; these are generally manageable and reversible on discontinuation of treatment. However, more severe toxicities have been reported, including acute kidney injury, glomerular and/or vascular injury such as thrombotic microangiopathy, and more rarely tubulointerstitial damage. Prescribing physicians should be aware of these potentially serious adverse effects. This article describes the mechanisms of action of antiangiogenic agents and their potential toxicities, with a particular focus on the kidneys.