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女性尿钠与尿钙之间关系的本质及意义。

The nature and significance of the relationship between urinary sodium and urinary calcium in women.

作者信息

Nordin B E, Need A G, Morris H A, Horowitz M

机构信息

Division of Clinical Chemistry, Institute of Medical and Veterinary Science, Adelaide, South Australia.

出版信息

J Nutr. 1993 Sep;123(9):1615-22. doi: 10.1093/jn/123.9.1615.

DOI:10.1093/jn/123.9.1615
PMID:8360790
Abstract

Orally or parenterally administered sodium is known to increase urinary calcium in experimental animals and humans, and there is well-documented correlation between urinary sodium and calcium in 24-h urine collections from normal subjects and renal stone formers. The correlation between urinary sodium and calcium is generally sodium driven, i.e., it is the sodium load that influences urinary calcium rather than vice versa, but the converse may also occur, as after an oral calcium load or in hypercalcemia. When sodium is the determinant, 100 mmol of sodium takes out approximately 1 mmol of calcium in the urine. When calcium load is the determinant, each millimole of calcium appearing in the urine is associated with an extra 10-20 mmol of sodium. Sodium-dependent calcium loss may continue indefinitely, but calcium-dependent natriuresis is self-limiting. There is a significant correlation between calcium and sodium in fasting urine from both pre- and postmenopausal women, but there is more calcium relative to sodium in postmenopausal women than in premenopausal women. In postmenopausal but not premenopausal women, urinary hydroxyproline is also related to obligatory sodium and calcium output, and restriction of salt intake lowers not only urinary sodium but also calcium and hydroxyproline. There is not only an increase in obligatory calcium excretion at the menopause, but also an increase in the fasting urinary sodium, which in turn accounts for some of the increase in calcium output. This rise in fasting urinary sodium represents a delay in sodium excretion that may have a significant effect on calcium homeostasis.

摘要

已知经口服或肠胃外途径给予的钠会增加实验动物和人类的尿钙排泄,并且在正常受试者和肾结石患者的24小时尿液收集样本中,尿钠与尿钙之间存在充分记录的相关性。尿钠与尿钙之间的相关性通常由钠驱动,即钠负荷影响尿钙排泄,而非相反,但也可能出现相反情况,如口服钙负荷后或处于高钙血症状态时。当钠起决定作用时,100 mmol的钠会使尿液中约排出1 mmol的钙。当钙负荷起决定作用时,尿液中每出现1 mmol的钙会伴有额外10 - 20 mmol的钠。钠依赖性钙流失可能会无限期持续,但钙依赖性利钠作用是自我限制的。绝经前和绝经后女性的空腹尿中钙与钠之间存在显著相关性,但绝经后女性尿中的钙相对于钠比绝经前女性更多。在绝经后女性而非绝经前女性中,尿羟脯氨酸也与必需的钠和钙排泄量相关,限制盐摄入不仅会降低尿钠排泄,还会降低尿钙和尿羟脯氨酸排泄。绝经时不仅会出现必需钙排泄增加,空腹尿钠也会增加,这反过来又导致了部分钙排泄量的增加。空腹尿钠的这种升高代表钠排泄延迟,这可能对钙稳态有显著影响。

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