Idiopathic Hypercalciuria and Nephrolithiasis
2011; Elsevier BV; Linguagem: Inglês
10.1016/b978-0-12-381978-9.10071-x
AutoresMurray J. Favus, Fredric L. Coe,
Tópico(s)Magnesium in Health and Disease
ResumoIdiopathic hypercalciuria is characterized by normocalcemia in the absence of known systemic causes of hypercalciuria. Intestinal calcium (Ca) absorption is almost always increased, and serum 1,25(OH)2D levels are elevated in some but not all patients. Idiopathic hypercalciuria (IH) affects 5 to 7% of adults and children and is the single most common cause of Ca oxalate kidney stone formation and also causes low bone mass. All of the metabolic features of IH can be reproduced by the administration of calcitriol to normal adults. There is also evidence of 1,25(OH)2D3 overproduction in some IH subjects. Excess 1,25(OH)2D3 action appears responsible for the intestinal Ca hyperabsorption, increased bone resorption, and decreased renal tubule Ca reabsorption. Serum 1,25(OH)2D3 is elevated in about 60% of patients. Patients with normal serum 1,25(OH)2D3 levels have comparable elevations in intestinal Ca absorption, and the possibility of elevated tissue vitamin D receptor found in GHS rats is suggested by one study in IH subjects which found elevated peripheral blood monocyte levels. Further, GHS rats and IH patients share changes in Ca transport in intestine, bone, and kidney. The GHS model of human IH permits studies of the cellular and molecular mechanisms of hypercalciuria found in humans. In this model, increased levels of VDR protein in duodenum, kidney, and bone may explain the hyperabsorption of Ca, increased bone resorption, and decreased renal tubule Ca reabsorption even in the presence of normal circulating concentrations of 1,25D.
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