Purpose of review
Changes in extracellular calcium concentration affect several functions of the renal tubule. The calcium-sensing receptor (CaSR), initially identified in the parathyroid gland cells, is also expressed in the kidney and was assumed to mediate all effects of extracellular calcium on the renal tubule. The purpose of this review is to critically review the evidence supporting this assumption.
Recent results confirm that, in the kidney, the CaSR is mainly expressed in the thick ascending limb of the loop of Henle. There, it is involved in the control of calcium reabsorption, independently of its action on parathyroid hormone secretion, through an effect on the paracellular pathway permeability. Although extracellular calcium affects transports other than that of calcium, the direct evidence that CaSR is involved in these effects is still lacking in many instances.
As the CaSR in the kidney controls calcium reabsorption and excretion and subsequently affects blood calcium concentration, agonists and antagonists of the CaSR could be used to control blood calcium concentration in patients who have lost their ability to regulate parathyroid hormone secretion. In addition, more work is needed to further decipher the molecular mechanisms through which CaSR determines calcium transport in the loop of Henle.