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lüll Vitamin D and calcium receptors: links to hypercalciuria Bai S; Favus MJCurr Opin Nephrol Hypertens 2006[Jul]; 15 (4): 381-5PURPOSE OF REVIEW: In idiopathic hypercalciuria, patients have increased intestinal Ca absorption and decreased renal Ca reabsorption, with either elevated or normal serum levels of 1,25-dihydroxyvitamin D. As 1,25-dihydroxyvitamin D exerts its biologic effects through interactions with the vitamin D receptor, we examine the actions of this receptor and 1,25-dihydroxyvitamin D in animals with genetic hypercalciuria. RECENT FINDINGS: In genetic hypercalciuric stone-forming rats intestinal calcium transport is increased and renal calcium reabsorption is reduced, yet serum 1,25-dihydroxyvitamin D levels are normal. Elevated intestinal and kidney vitamin D receptors suggest that increased tissue 1,25-dihydroxyvitamin D-vitamin D receptor complexes enhance 1,25-dihydroxyvitamin D actions on intestine and kidney, and vitamin D-dependent over-expression of renal calcium-sensing receptor alone can decrease tubule calcium reabsorption. In TRPV5-knockout mice, ablation of the renal calcium-influx channel decreases tubular calcium reabsorption, and secondary elevations in 1,25-dihydroxyvitamin D increase intestinal calcium transport. SUMMARY: 1,25-Dihydroxyvitamin D or vitamin D receptor may change intestinal and renal epithelial calcium transport simultaneously or calcium-transport changes across renal epithelia may be primary with a vitamin D-mediated secondary increase in intestinal transport. The extent of homology between the animal models and human idiopathic hypercalciuria remains to be determined.|Animals[MESH]|Biological Transport/genetics[MESH]|Calcitriol/*metabolism[MESH]|Calcium Channels/deficiency/*metabolism[MESH]|Calcium Metabolism Disorders/genetics/*metabolism[MESH]|Epithelium/metabolism[MESH]|Humans[MESH]|Kidney Diseases/genetics/*metabolism[MESH]|Kidney/*metabolism[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Rats[MESH]|Receptors, Calcium-Sensing/genetics/*metabolism[MESH]|TRPV Cation Channels/deficiency/*metabolism[MESH] |