title: Pathogenesis of hypercalciuric nephrolithiasis.
abstract: The major contribution of hypercalciuria in raising urinary state of saturation with respect to calcium salts and subsequent risk of nephrolithiasis is appreciated. Derangements in the physiological mechanisms that regulate calcium homeostasis and contribute to hypercalciuria have also been identified. New avenues of research are beginning to explore the specific defects that may contribute to hypercalciuria. From such studies, an understanding of the role of certain dietary excesses as contributors to the development of hypercalciuria and, in some cases, attendant bone loss, is beginning. The contribution of genetics to hypercalciuria has provided a powerful means of identifying genes that contribute to the hypercalciuric phenotype in a number of hypercalciuric conditions. Such studies have disclosed that hypercalciuria is probably polygenic in nature and will require a concerted effort to better understand the defects while attempting to develop gene-specific countermeasures.
authors.affiliation: Department of Internal Medicine, Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-8885, USA. joseph.zerwekh@utsouthwestern.edu
authors.forename: Joseph E
authors.initials: JE
authors.lastname: Zerwekh
authors.forename: Berenice Y
authors.initials: BY
authors.lastname: Reed-Gitomer
authors.forename: Charles Y C
authors.initials: CY
authors.lastname: Pak
mesh_terms: D002118:Calcium / Q000378:metabolism* / Q000652:urine; D006801:Humans; D007669:Kidney Calculi / Q000209:etiology* / Q000235:genetics / Q000378:metabolism; D020347:Lithiasis / Q000209:etiology* / Q000235:genetics / Q000378:metabolism; D010070:Oxalates / Q000378:metabolism / Q000652:urine
chemical_list: D010070:Oxalates; D002118:Calcium