Emerging role for fetuin-A as contributor to morbidity and mortality in chronic kidney disease

Abstract

Vascular calcification (VC) is an important reason for the high burden of vascular disease among chronic dialysis patients. Chronic kidney disease (CKD) is associated with increased promoters and decreased inhibitors of VC. The circulating levels of fetuin-A, a well-described inhibitor of calcification, regulate the cell-dependent process of osteogenesis. It is not surprising that the low circulating fetuin-A levels are associated with a greater prevalence and/or severity of VC and increased risk for all-cause and cardiovascular mortality. However, high circulating fetuin-A levels appear to induce insulin resistance and, in non-dialyzed subjects with diabetic nephropathy, are directly related to VC burden. These findings underscore the need to further clarify the multiple, systemic effects of fetuin-A and its role in health and various stages of CKD.