Abstract

The inhibitory effect of cinacalcet hydrochloride (cinacalcet) on blood phosphorus (P) levels is widely-accepted. However, this effect is only observed in patients on dialysis. Reduction in parathyroid hormone (PTH) induced by cinacalcet increases blood P levels with decreased urinary P excretion in pre-dialysis patients with chronic kidney disease (CKD). Similar results observed in normal and CKD rats provide a pharmacological validation of the trade-off hypothesis. The lowering effect of cinacalcet on blood P levels in dialysis patients is attributed to decreased P mobilization from the bone caused by the decreased PTH secretion. It is unlikely that this P-lowering effect of cinacalcet would bring any benefits on the enhanced parathyroid gland function and bone metabolism. On the other hand, the P-lowering effect of this drug is considered to contribute to its inhibitory effects on the development and progression of vascular calcification in dialysis patients. Further studies should examine this beneficial cinacalcet effect would lead to the reduction of the mortality risk.

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