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Acidosis and Urinary Calcium Excretion: Insights from Genetic Disorders.
Alexander, R Todd; Cordat, Emmanuelle; Chambrey, Régine; Dimke, Henrik; Eladari, Dominique.
Afiliación
  • Alexander RT; Departments of Pediatrics and todd2@ualberta.ca.
  • Cordat E; Physiology, University of Alberta, Edmonton, Canada.
  • Chambrey R; Physiology, University of Alberta, Edmonton, Canada.
  • Dimke H; Institut National de la Santé et de la Recherche Médicale U970, Paris Centre de Recherche Cardiovasculaire, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
  • Eladari D; Department of Cardiovascular and Renal Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Demark; and.
J Am Soc Nephrol ; 27(12): 3511-3520, 2016 Dec.
Article en En | MEDLINE | ID: mdl-27468975
Metabolic acidosis is associated with increased urinary calcium excretion and related sequelae, including nephrocalcinosis and nephrolithiasis. The increased urinary calcium excretion induced by metabolic acidosis predominantly results from increased mobilization of calcium out of bone and inhibition of calcium transport processes within the renal tubule. The mechanisms whereby acid alters the integrity and stability of bone have been examined extensively in the published literature. Here, after briefly reviewing this literature, we consider the effects of acid on calcium transport in the renal tubule and then discuss why not all gene defects that cause renal tubular acidosis are associated with hypercalciuria and nephrocalcinosis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Acidosis / Calcio / Túbulos Renales Tipo de estudio: Etiology_studies Límite: Humans Idioma: En Revista: J Am Soc Nephrol Asunto de la revista: NEFROLOGIA Año: 2016 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Acidosis / Calcio / Túbulos Renales Tipo de estudio: Etiology_studies Límite: Humans Idioma: En Revista: J Am Soc Nephrol Asunto de la revista: NEFROLOGIA Año: 2016 Tipo del documento: Article Pais de publicación: Estados Unidos