We evaluated serum gastrin, acid-base status, variables of mineral metabolism in fasting blood, as well as pH, relative supersaturation of stone forming constituents, and crystalluria in the associated fasting urine, of control subjects (n = 12), and in age- and weight-matched male normocalciuric (n
Fasting urine excretion of magnesium, calcium, and sodium in patients with renal calcium stones
β Scribed by Schwille, P.O. ;Schlenk, I. ;Samberger, N.M. ;Bornhof, C.
- Publisher
- Springer
- Year
- 1976
- Tongue
- English
- Weight
- 824 KB
- Volume
- 4
- Category
- Article
- ISSN
- 0300-5623
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β¦ Synopsis
Urine excretion of magnesium (Mg), calcium (Ca) and sodium(Na) was studied in patients with renal Ca stones having normal kidney function (n= 60), and in matched controls (n= 60), on a free diet following an overnight fasting period. In some formers, Mg was lower than in normals, whereas Ca was unusually high resulting in a significantly higher molar Ca/Mg ratio (p less than 0.001). 2. In 3 out of 4 stone groups Na excretion was significantly elevated because of reduced tubular reabsorption. In normals, fractional Na excretion varied between 0.44 and 0.54% of endogenous creatinine clearance, whereas it exceeded 1% in the stone patients. Conversely, the molar ratio Na/Ca was equal in all groups. 3. Fasting urinary cyclic AMP was comparable in both populations supporting the assumption that in the majority of patients Ca- or Mg- wasting via urine may not be responsible for secondary hyperparathyroidism. In small selected groups, losses of divalent cations may act in concert, leading to stimulation of the parathyroid glands. 4. Correlations between minerals and Na reveal a close relationship between Na, Ca and Mg in terms of clearance and excretion rate in patients and controls. Fractional Na and Ca excretion are correlated in patients but not in normals. This suggests that in the absence of phosphaturia, factors other than extracellular volume expansion and/or hyperparathyroidism are operative in stone disease. 5. The origin of fasting natriuresis and relative hypercalciuria may be ascribed to a change, as yet not causally identified, in distal tubular Na reabsorption.
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