Role of the calcium-sensing receptor in reducing the risk for calcium stones

Kirsten Y. Renkema, René J.M. Bindels, Joost G.J. Hoenderop

Research output: Contribution to journalArticleAcademicpeer-review

13 Citations (Scopus)


The tight control of blood Ca 2+ levels within a narrow range is essential for the performance of vital physiologic functions. Muscle contraction, neuronal excitation, and intracellular signaling processes acquisitively require Ca 2+. It is the concerted action of intestine, bone, and kidney that controls the Ca 2+ balance through the regulation of intestinal absorption, bone (de)mineralization, and renal excretion of Ca 2+, respectively. Along the nephron, fine-tuning of blood Ca 2+ levels takes place by Ca 2+ reabsorption. The calciotropic hormones regulate Ca 2+ transport processes, leading to whole-body Ca 2+ homeostasis and, importantly, preserving a constant Ca 2+ concentration in the blood. Defects in renal Ca 2+ handling can lead to hypercalciuria, consecutive kidney stone formation, and obstructive nephropathy. Here we give an overview of the key players involved in normal Ca 2+ management and describe the in-depth investigations on a renal hypercalciuric model of disease, the Trpv5 knockout mouse, which naturally displays molecular adaptations that prevent Ca 2+ precipitation in the kidney.

Original languageEnglish
Pages (from-to)2076-2082
Number of pages7
JournalClinical Journal of the American Society of Nephrology
Issue number8
Publication statusPublished - 1 Aug 2011


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