Activation of the Calcium Receptor by Calcimimetic Drugs – Physician's Weekly

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Apr 1, 2022
Phosphorus levels in the clinical range found in dialysis patients have been shown to reduce calcium receptor activation and affect parathyroid hormone (PTH) production from isolated parathyroid glands in vitro. As a result, some doctors and dialysis providers advised that calcimimetic medications are ineffective and should not be used to treat secondary hyperparathyroidism in dialysis patients whose serum phosphorus concentrations surpass specific threshold values.
For a study, researchers used data from large clinical trials to examine the effects of etelcalcetide and cinacalcet on plasma PTH levels in hemodialysis patients with secondary hyperparathyroidism and varying degrees of hyperphosphatemia to see if hyperphosphatemia reduces the therapeutic response to calcimimetic agents. 
Regardless of the degree of hyperphosphatemia at baseline, plasma PTH levels decreased gradually over the course of 26 weeks of therapy with etelcalcetide or cinacalcet. The reductions in PTH from baseline with each calcimimetic drug were smaller at each interval of follow-up during the trials among persons with blood phosphorus levels over one of three prespecified threshold values compared to those with serum phosphorus levels below these thresholds.
These data in vivo were the first in people to support the hypothesis that hyperphosphatemia reduces calcium receptor activation by calcium ions and calcimimetic drugs. However, the effect of hyperphosphatemia on calcimimetic drug responsiveness appeared to be minor and unlikely to be clinically important. Despite significant rises in blood phosphorus, the effectiveness of calcimimetic medications in decreasing plasma PTH levels in people with secondary hyperparathyroidism remained strong.
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