Abstract
Introduction: Cinacalcet (CNL) suppresses the secretion of parathyroid hormone (PTH). Objective: To consider the effect of CNL administration on achievement of K/DOQITM (Kidney Disease Outcomes Quality Initiative) targets in a group of hemodialysis (HD) patients with secondary hyperparathyroidism (SHPT). Patients and Methods: Patients undergoing HD who had initiated CNL enrolled in the study. Data were collected at the baseline and after 12 months. This data consisted of serum calcium (Ca), phosphorus (P), intact PTH (iPTH), proportion of calcium in dialysate, administered doses of CNL and proportion of administered phosphate binders and proportion of patients attaining K/DOQITM targets were gathered. Results: Twenty HD patients enrolled in the study. The proportions of individuals attaining K/DOQITM targets at month 12 were 35% for iPTH, 65% for P, 60% for Ca and 80% for Ca×P product, compared with 0%, 45%, 55% and 50% at the baseline respectively. Around 35% of individuals had attained the combined K/DOQITM targets for Ca, P and iPTH compared with 0% at the starting point. Conclusion: CNL ameliorates attainment of K/DOQITM targets in individuals with SHPT. This result is consistent with findings from other studies.
Highlights
Secondary hyperparathyroidism (SHPT) is a common complication of end-stage renal disease (ESRD)
The guidelines for the management of hyperparathyroidism in ESRD compiled by K/DOQITM was formulated based on work published up until 2001, before calcimimetics was available
Diminution of the Ca×P product is a desirable aspect of calcimimetic treatment and would accelerate attainments to reach to the targets for correction of secondary hyperparathyroidism (SHPT) [13]
Summary
Secondary hyperparathyroidism (SHPT) is a common complication of end-stage renal disease (ESRD). Only a small proportion of dialysis individuals with SHPT receiving regular treatments (Ca salts, vitamin D sterols and phosphate binders) reach and maintain control of these targets [7]. Calcimimetic agents increase the sensitivity of the Ca receptors of parathyroid cells to extracellular Ca ions, to inhibit the release of PTH, and to decrease PTH levels within a few hours after administration [10,11]. This mechanism of action differs fundamentally from that of vitamin D, which decreases the transcription of the PTH gene and hormone synthesis over a period of many hours
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