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
相关论文
共 133 条
  • [121] OSTEOPETROSIS ASSOCIATED WITH PROXIMAL AND DISTAL TUBULAR-ACIDOSIS
    VAINSEL, M
    ROCMANS, C
    FONDU, P
    GEPTS, W
    CADRANEL, S
    [J]. ACTA PAEDIATRICA SCANDINAVICA, 1972, 61 (04): : 429 - &
  • [122] The epithelial Ca2+ channel TRPV5 is essential for proper osteoclastic bone resorption
    van der Eerden, BCJ
    Hoenderop, JGJ
    de Vries, TJ
    Schoenmaker, T
    Buurman, CJ
    Uitterlinden, AG
    Pols, HAP
    Bindels, RJM
    van Leeuwen, JPTM
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (48) : 17507 - 17512
  • [123] Report of a family with two different hereditary diseases leading to early nephrocalcinosis
    Vargas-Poussou, Rosa
    Cochat, Pierre
    Le Pottier, Nelly
    Roncelin, Isabelle
    Liutkus, Aurelia
    Blanchard, Anne
    Jeunemaitre, Xavier
    [J]. PEDIATRIC NEPHROLOGY, 2008, 23 (01) : 149 - 153
  • [124] Mice lacking renal chloride channel, CLC-5, are a model for Dent's disease, a nephrolithiasis disorder associated with defective receptor-mediated endocytosis
    Wang, SS
    Devuyst, O
    Courtoy, PJ
    Wang, XT
    Wang, H
    Wang, YS
    Thakker, RV
    Guggino, S
    Guggino, WB
    [J]. HUMAN MOLECULAR GENETICS, 2000, 9 (20) : 2937 - 2945
  • [125] Atypical distal renal tubular acidosis confirmed by mutation analysis
    Weber, S
    Soergel, M
    Jeck, N
    Konrad, M
    [J]. PEDIATRIC NEPHROLOGY, 2000, 15 (3-4) : 201 - 204
  • [126] OSTEOPETROSIS, RENAL TUBULAR-ACIDOSIS AND BASAL GANGLIA CALCIFICATION IN 3 SISTERS
    WHYTE, MP
    MURPHY, WA
    FALLON, MD
    SLY, WS
    TEITELBAUM, SL
    MCALISTER, WH
    AVIOLI, LV
    [J]. AMERICAN JOURNAL OF MEDICINE, 1980, 69 (01) : 64 - 74
  • [127] EFFECTS OF ACUTE CHANGES IN ACID-BASE BALANCE ON RENAL CALCIUM EXCRETION IN DOGS
    WILLIAMSON, BJ
    FREEMAN, S
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1957, 191 (02): : 384 - 387
  • [128] WINSNES A, 1979, ACTA PAEDIATR SCAND, V68, P861
  • [129] WONG NLM, 1985, J LAB CLIN MED, V105, P472
  • [130] Role of NHE3 in mediating renal brush border Na+-H+ exchange - Adaptation to metabolic acidosis
    Wu, MS
    Biemesderfer, D
    Giebisch, G
    Aronson, PS
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (51) : 32749 - 32752
567891011121314