Acidosis and Urinary Calcium Excretion: Insights from Genetic Disorders

被引：59
作者：
Alexander, R. Todd [1 ,2 ]
Cordat, Emmanuelle [2 ]
Chambrey, Regine [3 ]
Dimke, Henrik [4 ]
Eladari, Dominique [3 ,5 ]
机构：
[1] Univ Alberta, Dept Pediat, Edmonton, AB, Canada
[2] Univ Alberta, Dept Physiol, Edmonton, AB, Canada
[3] Univ Paris 05, Sorbonne Paris Cite, Paris Ctr Rech Cardiovasc, Inst Natl Sante & Rech Med U970, Paris, France
[4] Univ Southern Denmark, Inst Mol Med, Dept Cardiovasc & Renal Res, Odense, Denmark
[5] Hop Europeen Georges Pompidou, Assistance Publ Hop Paris, Dept Physiol, Paris, France
来源：
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | 2016年 / 27卷 / 12期
基金：
加拿大健康研究院;
关键词：
RENAL TUBULAR-ACIDOSIS; ANHYDRASE-II DEFICIENCY; AUTOSOMAL RECESSIVE SYNDROME; REDUCED BONE THICKNESS; METABOLIC-ACIDOSIS; PARATHYROID-HORMONE; MICE LACKING; FUNCTIONAL-ANALYSIS; SODIUM-BICARBONATE; INTERCALATED CELLS;
D O I：
10.1681/ASN.2016030305
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
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.
引用
收藏
页码：3511 / 3520
页数：10
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