Rajesh jhaveri biography of barack

Introduction

Vascular endothelial growth factor signaling pathway inhibitors (VSPIs) treat numerous types of cancers by blocking tumor angiogenesis;¹ however, they are associated with both hypertension and proteinuria. Hypertension has been reported in 20% to 90% of patients.^2,3 The onset of hypertension can vary from hours to weeks, depending upon the half-life of the VSPI.⁴ Proposed mechanisms for VSPI-associated hypertension include reduced vasodilatory nitric oxide and prostacyclin, increased peripheral vascular resistance due to increased vasoconstrictive endothelin-1, and development of renal-limited thrombotic microangiopathy. Although it may serve as a marker of antiangiogenic action and treatment efficacy,S1 severe hypertension can contribute to cardiovascular morbidity and mortality, leading to interruption or discontinuation of VSPIs.⁵

Proteinuria can also occur with VSPI therapy in 21% to 63% of treated patients,⁵ and is thought to occur via rarefaction of the peritubular capillary network and disruption of the paracrine signaling between the podocyte and glomerular endothelium. Like VSPI-associated hypertension, proteinuria is associated with cardiovascular disease and poor patient outcomes, necessitating frequent monitoring after starting VSPIs.⁶

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