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Updated: Apr 19, 2026

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
Published on: June 2, 2022
Calcium-sensing receptor activation in chronic kidney disease: effects beyond parathyroid hormone control
Ziad A Massy1, Lucie Hénaut2, Tobias E Larsson3
1Inserm U-1088, University of Picardie Jules Verne, Amiens, France; Division of Nephrology, Ambroise Paré Hospital, Paris-Ile-de-France-Ouest University (University of Versailles Saint-Quentin-En-Yvelines), Paris-Boulogne Billancourt, France.
Abstract:
Secondary hyperparathyroidism (SHPT) is an important complication of advanced chronic kidney disease (CKD). Cinacalcet, an allosteric modulator of the calcium-sensing receptor (CaSR) expressed in parathyroid glands, is the only calcimimetic approved to treat SHPT in patients on dialysis. By enhancing CaSR sensitivity for plasma extracellular calcium (Ca(2+)0), cinacalcet reduces serum parathyroid hormone, Ca(2+)0, and serum inorganic phosphorous concentrations, allowing better control of SHPT and CKD-mineral and bone disorders. Of interest, the CaSR also is expressed in a variety of tissues where its activation regulates diverse cellular processes, including secretion, apoptosis, and proliferation. Thus, the existence of potential off-target effects of cinacalcet cannot be neglected. This review summarizes our current knowledge concerning the potential role(s) of the CaSR expressed in various tissues in CKD-related disorders, independently of parathyroid hormone control.
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