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Vascular endothelial growth factor (VEGF) signaling pathway inhibitors (VSPIs) treat numerous types of cancers by blocking tumor angiogenesis,1 yet are associated with both hypertension and proteinuria. Hypertension is one of the earliest on-target effects of VSPIs and has been reported in 20-90% of patients.2,3 The onset of hypertension can vary from hours to weeks, depending upon the half-life of the VSPI.4 There are several proposed mechanisms for VSPI-associated hypertension, including reduced vasodilatory nitric oxide and prostacyclin; increased peripheral vascular resistance due to increased vasoconstrictive endothelin-1; and development of renal-limited thrombotic microangiopathy (TMA).
Hanna et al. (Wed,) studied this question.