Alexander R Todd, Cordat Emmanuelle, Chambrey Régine, Dimke Henrik, Eladari Dominique
Departments of Pediatrics and
Physiology, University of Alberta, Edmonton, Canada.
J Am Soc Nephrol. 2016 Dec;27(12):3511-3520. doi: 10.1681/ASN.2016030305. Epub 2016 Jul 28.
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.
代谢性酸中毒与尿钙排泄增加及相关后遗症有关,包括肾钙质沉着症和肾结石。代谢性酸中毒引起的尿钙排泄增加主要是由于骨钙动员增加和肾小管内钙转运过程受到抑制。酸改变骨完整性和稳定性的机制已在已发表的文献中得到广泛研究。在此,在简要回顾这些文献后,我们考虑酸对肾小管钙转运的影响,然后讨论为什么并非所有导致肾小管酸中毒的基因缺陷都与高钙尿症和肾钙质沉着症有关。