Chronic kidney failure involves abnormalities of mineral metabolism, skeletal and of cardiovascular system (so called CKD – MBD) that have a major impact on the survival of renal patient. Increasingly complex pathophysiological mechanisms have been discovered in recent years with evidence of new molecules involved in the development of CKD – MBD. Besides the classical PTH / Vitamin D axis, the most recent discovery of a new FGF23 / Klotho axis has expanded knowledge on the mechanisms of mineral homeostasis but also on the more complex mechanisms of cellular aging, vascular calcification and cardiac remodeling. The importance of bone as an endocrine organ has become even more evident following the discovery of molecules such as Sclerostin (involved in the regulation of osteoblastic proliferation and differentiation) and Sibling (a family of proteins that regulate both local and systemic mineral metabolism). The ability to characterize as biomarkers of CKD – MBD for these new molecules depends on their eventual ability to express a specific pathophysiological processes, identify patients at risk, highlight the response to a therapeutic treatment and to be easily identifiable and quantifiable on biological fluids. As of today, it seems that we can recognize FGF23 as a biomarker of CKD-MBD, while the remaining molecules as still waiting for a more definite settlement.
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