Current Rheumatology Reports

, Volume 8, Issue 1, pp 70–75

Idiopathic hypercalciuria

  • Scott E. Liebman
  • Jeremy G. Taylor
  • David A. Bushinsky
Article

DOI: 10.1007/s11926-006-0029-z

Cite this article as:
Liebman, S.E., Taylor, J.G. & Bushinsky, D.A. Curr Rheumatol Rep (2006) 8: 70. doi:10.1007/s11926-006-0029-z

Abstract

Hypercalcuria is the most common metabolic disorder found in patients with nephrolithiasis. As the prevalence of kidney stones rises in industrialized nations, understanding the pathogenesis and treatment of hypercalciuria becomes increasingly important. Idiopathic hypercalciuria (IH), defined as an excess urine calcium excretion without an apparent underlying etiology, is the most frequent cause of hypercalciuria and will be the focus of this paper. Calcium homeostasis is tightly controlled and slight disturbances in transport at the level of the intestine, bone, and/or kidney can lead to excessive urine calcium excretion and promote stone formation. IH is a systemic disorder with dysregulation of calcium transport at a combination of these calcium regulatory sites. The goal of treatment is to prevent stone formation and relies on a 25combination of dietary and pharmaceutical interventions. Dietary management includes increasing fluid intake, salt restriction, animal protein restriction, and maintaining a normal calcium intake. Thiazide diuretics have proven effective in preventing calcium stone formation by reducing the urinary excretion of calcium. It is important to note that while decreasing urinary calcium excretion is important the clinician should focus primarily on reducing the supersaturation of calcium oxalate as this determines the true tendency for stone formation.

Copyright information

© Current Science Inc 2006

Authors and Affiliations

  • Scott E. Liebman
    • 1
  • Jeremy G. Taylor
  • David A. Bushinsky
  1. 1.Nephrology Division, Strong Memorial HospitalUniversity of Rochester School of Medicine and DentistryRochesterUSA