BMP4 and hyperphosphatemia: Key mechanisms include osteoblastic differentiation of vascular smooth muscle cells (induced by hyperphosphatemia, uremic toxins, and oxidative stress); deficiency of physiological calcification inhibitors such as fetuin-A, osteoprotegerin, and matrix Gla protein (which is vitamin K-dependent); and activation of pro-calcific pathways, including the transcription factor NFκB, bone morphogenetic protein-4 (BMP-4), and osteopontin [4-6,8].