“…The possible contributing factors in the pathophysiology of OHSS are increased secretion or exudation of protein-rich fluid from enlarged ovaries or peritoneal surfaces, increased follicular fluid levels of prorenin and renin (21), increased angiotensin-mediated changes in capillary permeability (22), and finally increased vascular endothelial growth factor, which is an angiogenic cytokine known to be a potent stimulator of the vascular endothelium (23). Furthermore, vascular endothelial growth factor (VEGF) appears to play an integral role in follicular growth, corpus luteum function, and ovarian angiogenesis (12,23).…”