title: Pathogenesis and management of hypercalciuric nephrolithiasis.
abstract: Hypercalciuria has long been recognized as an important metabolic derangement associated with the formation of calcareous renal stones. Hypercalciuria increases the saturation of the urine with respect to stone-forming salts and reduces inhibitor activity. There is now ample evidence that 'idiopathic hypercalciuria' is a heterogeneous disorder, comprising several entities including absorptive, renal and resorptive forms of hypercalciuria. Absorptive hypercalciuria is the most common variety, and recent studies suggest that in a large subset of these patients, increased intestinal calcium absorption is caused by increased production of calcitriol or greater sensitivity to calcitriol (e.g. upregulation of vitamin D receptors). Reduced spinal bone density found in these patients may relate to increased action of calcitriol on bone or to other factors. Since patients with vitamin D-dependent absorptive hypercalciuria may develop negative calcium balance when placed on diets restricted in calcium, therapy is shifting from severe dietary calcium restriction and sodium cellulose phosphate (calcium-binding resin) to thiazides and orthophosphates, which promote calcium retention. For each form of hypercalciuria, selective therapy should provide the best results.
authors.affiliation: Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center at Dallas 75235-8885, USA.
authors.forename: N A
authors.initials: NA
authors.lastname: Breslau
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000652:urine; D005260:Female; D006801:Humans; D007408:Intestinal Absorption; D007668:Kidney / Q000503:physiopathology; D007669:Kidney Calculi / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy*; D008297:Male; D009397:Nephrocalcinosis / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy*
chemical_list: D002118:Calcium