期刊
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
卷 27, 期 12, 页码 3511-3520出版社
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2016030305
关键词
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资金
- Women and Children Health Research Institute - Stollery Children's Hospital Foundation
- Canadian Institutes of Health Research
- Kidney Foundation of Canada
- Novo Nordisk Foundation
- Carlsberg Foundation
- Lundbeck Foundation
- A.P. Moller Foundation
- Lundbeck Foundation [R194-2015-1455] Funding Source: researchfish
- Novo Nordisk Fonden [NNF13OC0006513, NNF14OC0011749, NNF15OC0016096] Funding Source: researchfish
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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