Patterns of Urinary Calcium Excretion in Normal Subjects and in Renal Calculous Disease

1963 ◽  
Vol 89 (4) ◽  
pp. 541-545 ◽  
Author(s):  
J. Ernest Lathem ◽  
J. Stanton King
1971 ◽  
Vol 49 (5) ◽  
pp. 469-478 ◽  
Author(s):  
William H. Shaw

The relationship between urinary calcium excretion and serum calcium was studied at stable serum calcium levels, both normal and elevated. The linearity of this relationship being known, the slope of this line could be determined by sampling only at its lower and upper ends, that is, by measuring urine and serum calcium at a resting level and at a constant level of hypercalcemia produced by a calcium infusion. This method permitted three sets of measurements at each of the two levels, and also tended to eliminate the factor of renal delay time. The procedure was performed with normal subjects, with normals given vitamin D2 or parathyroid extract, and with subjects having hyperparathyroidism, sarcoidosis, and recurrent renal calculi. In the normal subjects the gradient of the slope appeared to indicate that there is no maximal tubular reabsorptive capacity for calcium, in the range sampled at any rate. The slopes of the various abnormal subjects mostly did not differ markedly from those of the normals. One incidental finding was that resting levels of urinary calcium excretion were significantly depressed 24 h following vitamin D2 administration, despite unchanged serum calcium levels.


1988 ◽  
Vol 75 (2) ◽  
pp. 203-207 ◽  
Author(s):  
Viroon Mavichak ◽  
Christopher M. L. Coppin ◽  
Norman L. M. Wong ◽  
John H. Dirks ◽  
Valerie Walker ◽  
...  

1. The renal handling of calcium and magnesium was studied in six patients with persistent hypomagnesaemia after cis-platinum treatment for testicular tumours. 2. In comparison with normal subjects, the patients showed hypomagnesaemia (mean 0.54 mmol/l), which was associated with a normal urinary magnesium excretion (mean 4.83 mmol/24 h). Urinary calcium excretion was significantly lower in the patients than in the normal subjects (mean 2.05 vs 5.15 mmol/24 h, respectively; P < 0.01), despite slightly higher total serum calcium levels (2.53 vs 2.38 mmol/l, respectively; P < 0.05). During magnesium chloride infusion, when serum magnesium levels were comparable in patients and controls, urinary calcium excretion remained lower in the patients, indicating that hypomagnesaemia was not the cause of the hypocalciuria. 3. Dietary magnesium supplementation resulted in a significant increase in the serum magnesium levels in the patients, while dietary magnesium deprivation resulted in a comparable decrease in urinary magnesium excretion in patients and controls (to 1.46 and 2.00 mmol/day, respectively), although the serum magnesium level fell further (to 0.46 mmol/l) in the patients. 4. The dissociation of renal calcium and magnesium excretion appears to be part of the intrinsic tubular defect caused by cis-platinum. This dissociation of urinary calcium and magnesium excretion, which resembles that seen in Bartter's syndrome, may result from a lesion in the distal convoluted tubule.


1989 ◽  
Vol 35 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D M Cowley ◽  
B C McWhinney ◽  
J M Brown ◽  
A H Chalmers

Abstract Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.


1970 ◽  
Vol 64 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Lars Runeberg ◽  
B.-A. Lamberg ◽  
P. Reissell ◽  
H. Adlercreutz

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.


1998 ◽  
Vol 18 (3) ◽  
pp. 475-487 ◽  
Author(s):  
Susan J Whiting ◽  
Timothy J Green ◽  
Evelyn P MacKenzie ◽  
Shawna J Weeks

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