Renal side effects of VEGF-blocking therapy

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Abstract
Neoangiogenesis is a necessary key event for tumour growth and metastatic dissemination. Vascular endothelial growth factor (VEGF) is produced by various tumours of a certain size to supply the cancer with new blood vessels. Production of VEGF is related to aggressiveness, metastatic potential and relapse of tumours [1]. Thus, anti-VEGF therapies that either block the extracellular binding of VEGF to its receptor (anti-VEGF antibodies) or inhibit intracellular signalling pathways of VEGF receptors (receptor tyrosine kinase inhibitors) have become an innovative target in the treatment of cancers. Bevacizumab is a humanized monoclonal antibody directed against VEGF-A. It is used as first-line treatment for patients with metastatic colorectal carcinoma [2]. Sunitinib (Sutent) is a VEGFR-2/-3 tyrosine kinase inhibitor approved by the Food and Drug Administration for the treatment of gastrointestinal stromal tumours and as first-line treatment for patients with metastatic renal cell cancer [3]. Even though anti-VEGF therapies are generally well tolerated, bleeding, hypertension and asymptomatic proteinuria are well-known side effects. Renal damage which is infrequently reported as proteinuria is usually reversible, but in some rare cases nephrotic-range proteinuria, acute renal dysfunction, interstitial nephritis and thrombotic microangiopathy were reported [4,5].

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