ight 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.
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