Pathogenesis and management of hypercalciuric nephrolithiasis.
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.
Breslau
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Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center at Dallas 75235-8885, USA.
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*
D002118:Calcium