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Journal of Clinical Endocrinology & Metabolism Vol. 48, No. 2 260-265
doi:10.1210/jcem-48-2-260
Copyright © 1979 by the Endocrine Society.
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Fasting Urinary Calcium and Adenosine 3',5'-Monophosphate: A Discriminant Analysis for the Identification of Renal and Absorptive Hypercalciurias*

CHARLES Y. C PAK and RICHARD A GALOSY

Section on Mineral Metabolism, Department of Internal Medicine, and the Department of Cell Biology, the University of Texas Health Science Center at Dallas, Southwestern Medical School Dallas, Texas, 75235

Address requests for reprints to: Dr. Charles Y. C. Pak, Department of Medicine, University of Texas Health Science Center at Dallas, Southwestern Medical School, 5323 Harry Hines Boulevard, Dallas, Texas 75235.

Fasting urinary calcium and cAMP were determined in 45 control subjects, 51 patients with absorptive hypercalciuria, and 20 patients with renal hypercalciuria. The mean fasting urinary Ca was significantly higher in absorptive hypercalciuria than in the control group [0.077 ± 0.026 vs. 0.053 ± 0.027 (SD) mg/100 ml glomerular filtration (GF); P < 0.001]. Although the mean fasting urinary Ca of 0.174 ± 0.060 mg/100 ml GF and the value for cAMP in renal hypercalciuria were both significantly higher than those in other groups, the individual values for fasting urinary cAMP overlapped widely into the ranges found in the control and absorptive hypercalciuria groups. In the control group, fasting urinary calcium was inversely correlated with fasting urinary cAMP (P < 0.05). Values in absorptive hypercalciuria were within 2 SES of estimate for the control group, though they were higher in calcium and lower in cAMP. When the contribution of absorbed calcium was reduced by prior administration of sodium cellulose phosphate, fasting urinary calcium significantly decreased and urinary cAMP significantly increased toward the range found in the control group. The results suggested that the inverse relationship found between fasting urinary calcium and cAMP in the control and absorptive hypercalciuria groups may be physiologically meaningful, and that the higher fasting urinary calcium in absorptive hypercalciuria may be the sequela of incomplete renal excretion of absorbed calcium.

In contrast, the relationship between fasting urinary calcium and cAMP in renal hypercalciuria did not resemble that in the control or absorptive hypercalciuria groups. A discriminant analysis of data from the control and renal hypercalciuria groups permitted the derivation of a Ca-cAMP discriminant score: fasting urinary Ca (23.9) + urinary cAMP (0.0507) – 3.0249, where Ca is expressed as milligrams per 100 ml GF and cAMP is expressed as nanomoles per 100 ml GF. This score completely discriminated between patients with renal hypercalciuria and the control subjects; all of the values in the renal hypercalciuria group were positive, while those in the control group were negative. In contrast, only one patient with absorptive hypercalciuria had a score which was within the range found in renal hypercalciuria. This finding supports the hypothesis that a primary renal leak of calcium is not present in the majority of patients with absorptive hypercalciuria. (J Clin EndocrinolMetab 48: 260,1979)

* This work was supported by grants from the USPHS (R01-AM16061,1-P50-AM20543, and 5-M01-RR-00633).

Received July 3, 1978.




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