{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T01:13:49Z","timestamp":1792631629248,"version":"4.5.0"},"reference-count":106,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2019,2]]},"abstract":"<jats:p>\n                    Inhibition of vascular endothelial growth factor A (VEGFA)\/vascular endothelial growth factor receptor 2 (VEGFR2) signaling is a common therapeutic strategy in oncology, with new drugs continuously in development. In this review, we consider the experimental and clinical evidence behind the diverse nephrotoxicities associated with the inhibition of this pathway. We also review the renal effects of VEGF inhibition\u2019s mediation of key downstream signaling pathways, specifically MAPK\/ERK1\/2, endothelial nitric oxide synthase, and mammalian target of rapamycin (mTOR). Direct VEGFA inhibition\n                    <jats:italic toggle=\"yes\">via<\/jats:italic>\n                    antibody binding or VEGF trap (a soluble decoy receptor) is associated with renal-specific thrombotic microangiopathy (TMA). Reports also indicate that tyrosine kinase inhibition of the VEGF receptors is preferentially associated with glomerulopathies such as minimal change disease and FSGS. Inhibition of the downstream pathway RAF\/MAPK\/ERK has largely been associated with tubulointerstitial injury. Inhibition of mTOR is most commonly associated with albuminuria and podocyte injury, but has also been linked to renal-specific TMA. In all, we review the experimentally validated mechanisms by which VEGFA-VEGFR2 inhibitors contribute to nephrotoxicity, as well as the wide range of clinical manifestations that have been reported with their use. We also highlight potential avenues for future research to elucidate mechanisms for minimizing nephrotoxicity while maintaining therapeutic efficacy.\n                  <\/jats:p>","DOI":"10.1681\/asn.2018080853","type":"journal-article","created":{"date-parts":[[2019,1,14]],"date-time":"2019-01-14T16:35:16Z","timestamp":1547483716000},"page":"187-200","source":"Crossref","is-referenced-by-count":209,"title":["Therapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities"],"prefix":"10.1681","volume":"30","author":[{"given":"Chelsea C.","family":"Estrada","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alejandro","family":"Maldonado","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandeep K.","family":"Mallipattu","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York; 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