Secondary hyperparathyroidism is characterized by an acclivity in parathyroid hormone (PTH) associated with bare levels of alive vitamin D hormone. The antecedent of vitamin D in the physique is from amalgam in the derma and from comestible intake. Vitamin D requires two consecutive hydroxylations in the alarmist and the branch to bind to and to actuate the vitamin D receptor (VDR). The autogenous VDR activator, calcitriol [1,25(OH)2 D3], is a hormone that binds to VDRs that are present in the parathyroid gland, intestine, kidney, and cartilage to advance parathyroid action and calcium and phosphorus homeostasis, and to VDRs begin in abounding added tissues, including prostate, endothelium and allowed cells. VDR activation is capital for the able accumulation and aliment of accustomed bone. In the afflicted kidney, the activation of vitamin D is diminished, consistent in a acceleration of PTH, after arch to accessory hyperparathyroidism and disturbances in the calcium and phosphorus homeostasis.1 Decreased levels of 1,25(OH)2 D3 accept been empiric in aboriginal stages of abiding branch disease. The decreased levels of 1,25(OH)2 D3 and resultant animated PTH levels, both of which generally announce abnormalities in serum calcium and phosphorus, affect cartilage about-face amount and may aftereffect in renal osteodystrophy. An in vitro abstraction indicates that paricalcitol is not an inhibitor of CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1 or CYP3A at concentrations up to 50 nM (21 ng/mL).