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Idiopathic hypercalciuria.
Curr Rheumatol Rep 2006; 8(1):70-5CR

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 combination 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.

Authors+Show Affiliations

University of Rochester School of Medicine and Dentistry, Nephrology Division, Strong Memorial Hospital, 601 Elmwood Avenue, Box 675, Rochester, NY 14642, USA. scott_liebman@urmc.rochester.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16515769

Citation

Liebman, Scott E., et al. "Idiopathic Hypercalciuria." Current Rheumatology Reports, vol. 8, no. 1, 2006, pp. 70-5.
Liebman SE, Taylor JG, Bushinsky DA. Idiopathic hypercalciuria. Curr Rheumatol Rep. 2006;8(1):70-5.
Liebman, S. E., Taylor, J. G., & Bushinsky, D. A. (2006). Idiopathic hypercalciuria. Current Rheumatology Reports, 8(1), pp. 70-5.
Liebman SE, Taylor JG, Bushinsky DA. Idiopathic Hypercalciuria. Curr Rheumatol Rep. 2006;8(1):70-5. PubMed PMID: 16515769.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Idiopathic hypercalciuria. AU - Liebman,Scott E, AU - Taylor,Jeremy G, AU - Bushinsky,David A, PY - 2006/3/7/pubmed PY - 2007/10/5/medline PY - 2006/3/7/entrez SP - 70 EP - 5 JF - Current rheumatology reports JO - Curr Rheumatol Rep VL - 8 IS - 1 N2 - 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 combination 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. SN - 1523-3774 UR - https://www.unboundmedicine.com/medline/citation/16515769/full_citation L2 - https://medlineplus.gov/kidneystones.html DB - PRIME DP - Unbound Medicine ER -