Fig. 2.
Mechanisms of vascular calcification in CKD patients. Disturbances of mineral and bone metabolism are common in patients with CKD. The progressive loss of kidney function is accompanied—among other changes—by elevated serum FGF23 levels, a decrease in inorganic phosphate excretion and a dysregulation of bone metabolism. These anomalies are intimately interrelated. Indicators of this disturbed state are pathological changes of various biomarkers such as OPG, Klotho, FGF23, PTH and calcitriol. Whether their altered serum levels are the cause or the consequence of the skeletal abnormalities requires further study. The resulting derangements in mineral metabolism, as reflected by altered serum and vascular tissue levels of Ca, Pi and Mg are accompanied by additional metabolic changes and inflammation. This leads to loss of circulating and/or local mineralization inhibitors such as fetuin A, PPi and MGP, further supporting the development of vascular calcification. Ca, calcium; FGF23, fibroblast growth factor 23; Mg, magnesium; MGP, matrix Gla protein; OPG, osteoprotegerin; Pi , inorganic phosphate; PPi, inorganic pyrophosphate; PTH, parathyroid hormone. (modified after Schoppet, Shroff et al. [17]).