Abstract
The classical pathogenesis of secondary hyperparathyroidism (SHPT) includes the disturbance of Ca, P, and calcitriol metabolisms as a result of decreased kidney function. SHPT is characterized by the increased biosynthesis and secretion of parathyroid hormone (PTH) and parathyroid cell proliferation. The abnormalities of the expression and function of calcium-sensing and vitamin D (VD) receptors are closely associated with the disease progression. Current treatment for SHPT includes phosphate binders and VD sterols. Although VD sterols are effective to suppress PTH, the dose is limited because of its calcemic and phosphatemic actions that may progress vascular calcification. The calcimimetic compound, a new device which selectively targets the CaSR has a positive impact on mineral metabolism and effectively suppresses PTH.
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