Pathophysiology of hypercalciuria.
The mechanisms responsible for hypercalciuria may involve intestinal calcium transport, renal tubule calcium reabsorption, and the regulation of bone mineral content. Both parathyroid hormone and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) may alter urine calcium. For these reasons, understanding the pathogenesis of hypercalciuria in patients has proven to be difficult. We present here an analysis of pathways that regulate systemic calcium homeostasis and of the various mechanisms that have been proposed to explain normocalcemic hypercalciuria in humans. Available evidence seems to implicate disordered regulation of 1,25(OH)2D3 as a basis for at least one common form of hypercalciuria.
D001581:Benzothiadiazines; D001842:Bone and Bones / Q000378:metabolism; D002117:Calcitriol / Q000378:metabolism; D002118:Calcium / Q000378:metabolism / Q000652:urine*; D002128:Calcium Metabolism Disorders / Q000235:genetics / Q000503:physiopathology* / Q000628:therapy; D002136:Calcium, Dietary / Q000008:administration & dosage; D004232:Diuretics; D006706:Homeostasis; D006801:Humans; D007408:Intestinal Absorption; D007669:Kidney Calculi / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D007684:Kidney Tubules / Q000378:metabolism; D010281:Parathyroid Hormone / Q000378:metabolism; D049993:Sodium Chloride Symporter Inhibitors / Q000627:therapeutic use
D001581:Benzothiadiazines; D002136:Calcium, Dietary; D004232:Diuretics; D010281:Parathyroid Hormone; D049993:Sodium Chloride Symporter Inhibitors; D002117:Calcitriol; D002118:Calcium