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THE DEPENDENCE OF URINARY CALCIUM AND OTHER ELECTROLYTES ON ADRENAL FUNCTION DURING ACUTE SODIUM DEPLETION AND LOADING
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ABSTRACT
The time course of the renal excretion of calcium, magnesium, sodium, and potassium during sodium depletion and the rapid correction of the extracellular volume deficit was studied in normal subjects and in patients with Addison's disease (AD). The decrease in body weight was similar in the two groups, but the haematocrit value increased more in the patients with AD.
Sodium depletion suppressed sodium excretion much more efficiently in normal controls than in the AD patients. Calcium excretion was roughly equally depressed in two groups. During sodium loading there was an immediate increase in renal sodium excretion in the patients with AD, whereas the sodium-retaining state generally continued for about one day in the normal controls. Urinary potassium decreased gradually during the first day of sodium loading in the normal controls but not in the AD patients. In the normal subjects calcium excretion remained low during the first day and increased on the second day of sodium loading. In the AD patients there was a gradual increase in urinary calcium during the first day of sodium loading, which did not, however, parallel the changes in urinary sodium content in individual urine samples. Urinary magnesium did not change significantly.
It is concluded that the effect of adrenal steroids on renal calcium excretion is of minor importance. They may, however, to some extent induce calcium retention.
Oxford University Press (OUP)
Title: THE DEPENDENCE OF URINARY CALCIUM AND OTHER ELECTROLYTES ON ADRENAL FUNCTION DURING ACUTE SODIUM DEPLETION AND LOADING
Description:
ABSTRACT
The time course of the renal excretion of calcium, magnesium, sodium, and potassium during sodium depletion and the rapid correction of the extracellular volume deficit was studied in normal subjects and in patients with Addison's disease (AD).
The decrease in body weight was similar in the two groups, but the haematocrit value increased more in the patients with AD.
Sodium depletion suppressed sodium excretion much more efficiently in normal controls than in the AD patients.
Calcium excretion was roughly equally depressed in two groups.
During sodium loading there was an immediate increase in renal sodium excretion in the patients with AD, whereas the sodium-retaining state generally continued for about one day in the normal controls.
Urinary potassium decreased gradually during the first day of sodium loading in the normal controls but not in the AD patients.
In the normal subjects calcium excretion remained low during the first day and increased on the second day of sodium loading.
In the AD patients there was a gradual increase in urinary calcium during the first day of sodium loading, which did not, however, parallel the changes in urinary sodium content in individual urine samples.
Urinary magnesium did not change significantly.
It is concluded that the effect of adrenal steroids on renal calcium excretion is of minor importance.
They may, however, to some extent induce calcium retention.
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