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Role of the calcium-sensing receptor in reducing the risk for calcium stones Renkema KY; Bindels RJ; Hoenderop JGClin J Am Soc Nephrol 2011[Aug]; 6 (8): 2076-82The tight control of blood Ca2+ levels within a narrow range is essential for the performance of vital physiologic functions. Muscle contraction, neuronal excitation, and intracellular signaling processes acquisitively require Ca2+. It is the concerted action of intestine, bone, and kidney that controls the Ca2+ balance through the regulation of intestinal absorption, bone (de)mineralization, and renal excretion of Ca2+, respectively. Along the nephron, fine-tuning of blood Ca2+ levels takes place by Ca2+ reabsorption. The calciotropic hormones regulate Ca2+ transport processes, leading to whole-body Ca2+ homeostasis and, importantly, preserving a constant Ca2+ concentration in the blood. Defects in renal Ca2+ handling can lead to hypercalciuria, consecutive kidney stone formation, and obstructive nephropathy. Here we give an overview of the key players involved in normal Ca2+ 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 Ca2+ precipitation in the kidney.|Adaptation, Physiological[MESH]|Animals[MESH]|Calcium Channels/deficiency/genetics[MESH]|Calcium/*metabolism/urine[MESH]|Crystallization[MESH]|Disease Models, Animal[MESH]|Homeostasis[MESH]|Humans[MESH]|Hypercalciuria/genetics/metabolism[MESH]|Kidney/*metabolism[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Nephrolithiasis/etiology/genetics/metabolism/*prevention & control[MESH]|Receptors, Calcium-Sensing/*metabolism[MESH]|TRPV Cation Channels/deficiency/genetics[MESH] |
