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Clinical Chemistry 45: 257-261, 1999;
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(Clinical Chemistry. 1999;45:257-261.)
© 1999 American Association for Clinical Chemistry, Inc.

Articles

Study of Calcium Metabolism in Idiopathic Hypercalciuria by Strontium Oral Load Test

Giuseppe Vezzolia, Andrea Caumo, Ivano Baragetti, Simona Zerbi, Piera Bellinzoni, Antonella Centemero, Alessandro Rubinacci, GianLuigi Moro, Donatella Adamo, Giuseppe Bianchi and Laura Soldati

a Address correspondence to this author at: Divisione Nefrologia, Dialisi e Ipertensione, Ospedale San Raffaele, Via Olgettina 60, 20132 Milano, Italy. Fax 2-26432384; e-mail vezzoli.giuseppe{at}hsr.it.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Calcium excretion and absorption were evaluated in hypercalciuric calcium stone formers by the study of Sr2+ excretion and absorption after an oral load. Ca2+ stone formers (n = 140) were studied, and the results were compared in the 83 of them who had idiopathic hypercalciuria and in the 57 who had Ca2+ excretion within reference values. Hypercalciuric patients showed increased renal Sr2+ clearance (CRE; 5.26 ± 0.358 vs 3.29 ± 0.277 mL/min; P <0.001), whereas Sr2+ absorption [assessed as the area under the serum concentration–time curve (AUC)] was increased at 30 and 60 min (1.53 ± 0.087 vs 1.21 ± 0.071 mmol · L-1 · min; P <0.05), but not at 240 min after the load. In hypercalciuric patients, the AUCs were positively correlated with urinary Sr2+ fractional excretion (P <0.001). Conversely, in normocalciuric patients plasma parathyroid hormone (PTH) was negatively correlated with the AUCs (P <0.01) and CRE (P <0.05), whereas 1,25-dihydroxyvitamin D plasma concentrations normalized to PTH were positively correlated with the AUCs (P <0.05). The results of Sr2+ load tests suggest that in the hypercalciuric population, Ca2+ absorption is altered predominantly in the duodenum and that the normal regulation exerted by calciotropic hormones on tubular and enteral Ca2+ handling is lost.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
Idiopathic hypercalciuria is a familial disorder clinically associated with kidney stone production and reduced bone mineral content (1)(2)(3). An increase of intestinal Ca2+ absorption and a reduction of tubular Ca2+ reabsorption are involved in the development of the disorder (4)(5)(6)(7)(8); however, their primary or secondary roles are difficult to define because of complex variable interrelationships. In addition, technical difficulties and possible hazards related to the use of Ca2+ isotopes have hampered the extensive study of enteral and tubular Ca2+ handling and the possibility to gain additional insight into the mechanisms leading to hypercalciuria. The increase of enteral Ca2+ absorption is considered the most common cause of idiopathic hypercalciuria (4)(5), although the specific cellular defect remains unknown. Its increase has been attributed to abnormally high 1,25-dihydroxyvitamin D [1,25(OH)2D3]1 production (6)(7) or to enteral sensitivity to 1,25(OH)2D3 (5)(8); however, it was not found to be correlated with the plasma concentrations of calciotropic hormones or urinary Ca2+ excretion. A tubular defect in phosphate reabsorption was hypothesized to stimulate 1,25(OH)2D3 synthesis and Ca2+ absorption (7)(8).

Because Sr2+ ions are handled in intestinal mucosa and kidney tubule by the same transport systems as Ca2+ ions (9)(10), intestinal Ca+ absorption and excretion can be analyzed using stable Sr2+ as a marker (11)(12). However, because Sr2+ transport is less efficient than Ca2+ transport in both organs, Ca2+ intestinal absorption and tubular reabsorption are underestimated when assessed using Sr2+ (10)(11). The oral Sr2+ load test, which takes 4 h, allows evaluation of the ion absorption in the duodenum, jejunum, and the first ileum segment and analysis of the initial part of ion urinary excretion, which continues for several days after the oral load (13)(14)(15).

Intestinal Sr2+ absorption was found to be well correlated with Ca2+ absorption (14) and appeared to be modulated by calciotropic hormones, similar to Ca2+ (15)(16)(17). In keeping with the current knowledge about Ca2+ metabolism, Sr2+ absorption in normocalciuric subjects was negatively correlated with plasma parathyroid hormone (PTH) and positively correlated with plasma 1,25(OH)2D3 when normalized to PTH concentrations (15). The enhancing effect of 1,25(OH)2D3 on intestinal absorption of both Ca2+ and Sr2+ ions was also shown after its oral administration (16)(17)(18); however its effect on Sr2+ absorption was lower than that on Ca2+ absorption (16). The regulation of urinary Sr2+ excretion has been poorly studied. A weak negative correlation between renal Sr2+ clearance (CRE) and plasma concentrations of PTH was observed in normocalciuric patients, indicating the control that PTH exerts similar on tubular Sr2+ reabsorption as on tubular Ca2+ transport (15). These findings suggest that Sr2+ handling can be a mirror of Ca2+ metabolism and can be used to monitor its alterations. In the present study, an oral Sr2+ load test was used to evaluate alterations of Ca2+ intestinal absorption and renal reabsorption in stone-forming patients with idiopathic hypercalciuria, as compared to normocalciuric stone formers.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
subjects
Patients with idiopathic Ca2+-oxalate nephrolithiasis (n = 140) were admitted to the study. Results obtained in 83 patients with idiopathic hypercalciuria [50 men and 33 women; weight, 68 ± 1.4 kg (73 ± 1.6 in men and 61 ± 2.0 in women); age, 46 ± 1.4 years] were compared with those obtained in 57 normocalciuric patients [30 men and 27 women; weight 68 ± 1.5 kg (76 ± 1.6 in men and 59 ± 1.5 in women); age, 43 ± 1.9 years]. Among the normocalciuric patients, 20 were studied for the first time, whereas 37 had participated to a previous study (15) and were included in this work because they had been submitted to the bone mineral density (BMD) determination. A normocalciuric patient with abnormally high urine Sr2+ clearance compared with the other normocalciuric subjects was not included in the study, as described previously (15). Patients were considered hypercalciuric when the 24-h Ca2+ excretion was >7.5 mmol in men or 6.25 mmol in women or >0.1 mmol/kg of body weight for both sexes. All patients were studied after 8 days on a diet containing ~25 mmol of Ca2+ per day, obtained by adjusting dairy product intake. Their plasma concentrations of Ca2+, phosphate, and creatinine were within the appropriate health-related reference intervals. They did not have diseases except kidney stones and did not take drugs. None had voiding difficulties. Among the women, 16 hypercalciuric (48–67 years of age) and 4 normocalciuric (51–65 years of age) subjects were postmenopausal, but none had been in therapy with antiosteoporotic drugs. They all gave informed consent for the study, which was approved by the San Raffaele Hospital Ethics Committee.

experimental protocol
The oral Sr2+ load test was performed as described previously (15). After an overnight fast, 30.2 µmol Sr2+/kg body weight (2.65 mg/kg body weight) were administered to patients in water solution [11.4 mmol/L (1 g/L)]. This solution was prepared from SrCl2·6 H2O (3.04 g/L; obtained from BDH). Blood samples were drawn before and at 30, 60, and 240 min after Sr2+ administration. Urine was collected 4 h after Sr2+ adminstration.

assays
Ca2+, phosphate, sodium, and creatinine were measured in plasma and 24-h urine. Intact PTH and 1,25(OH)2D3 were determined in plasma by immunoradiometric and radioreceptor assays, respectively (both from Nichols Institute). 1,25(OH)2D3 was determined in 27 normocalciuric and 37 hypercalciuric patients. The plasma values of 1,25(OH)2D3 were normalized to PTH plasma concentrations (1,25(OH)2D3/PTH) to obtain an index of 1,25(OH)2D3 production (19).

The Sr2+ concentration was measured by atomic absorption spectrophotometry at 460.7 nm (Perkin-Elmer 4000), using acetylene-air flame in 10-fold diluted serum and 50-fold diluted urine with 2 g/L lanthanum and 10 mL/L hydrochloric acid as the diluent.

BMD was assessed by dual energy x-ray absorptiometry (Hologic QDR 1000 or 4500W) at three femoral sites (the neck, the trochanter, and the Ward triangle) and L1–L4 lumbar spine vertebrae. The BMD values were expressed as the number of SD from the mean of a healthy young Caucasian population (t-score). Patients having t-scores lower than -2.5 were defined as osteoporotic; patients with t-score greater than -2.5 were defined as conventionally "normal", although this limit includes osteopenic patients with t-scores between -2.5 and -1. The coefficients of variation (CVs) for the instruments were calculated daily by quality-control scans of the spine phantom and were <0.5%.

calculations
Strontium absorption was calculated at 30, 60, and 240 min after the load as the incremental area under the serum concentration-time curve (AUC30, AUC60, and AUC240), determined by the trapezoid method and expressed as mmol · L-1 · min.

The renal Sr2+ excretion was expressed as the fraction of administered Sr2+ excreted in the urine collected at the end of the test (FE). CRE was quantified as the ratio of Sr2+ excreted during the test divided by the value for AUC240; it was expressed as mL/min. Calculations needed to obtain the indices of Sr2+ metabolism have been described in our previous work (15).

statistical analysis
Data are expressed in the text as means ± SE. Statistical differences of the means were analyzed by the Mann–Whitney U-test. Differences in frequency distributions between groups were compared by the {chi}2- test. Simple linear correlations between variables were analyzed. Serum Sr2+ concentration–time curves were compared by ANOVA for repeated measures.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
The hypercalciuric stone formers differed from the normocalciuric patients in their urinary excretion of Ca2+, Na+, and phosphate; the plasma concentrations of electrolytes and calciotropic hormones were within health-related reference intervals; their BMD values were not significantly low at the sites investigated (Table 1 ). Twenty-two (26.5%) hypercalciuric and 15 (26.3%) normocalciuric patients (P >0.05) were osteoporotic, having t-scores below -2.5 at least at one of the sites studied. The distribution of patient age could justify the high frequency of osteoporosis in the two populations: 36.1% of hypercalciuric patients (age range, 21–79 years) and 36.1% of normocalciuric patients (age range, 21–72 years) were >50.


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  		Table 1. Divalent ion metabolism indices in normocalciuric and hypercalciuric stone formers.

The results of the oral Sr2+ load test show a different Sr2+ absorption kinetic curve in the two patient groups (Fig. 1 ). The values of AUC30 and AUC60 were significantly higher in hypercalciuric patients, whereas the AUC240 increase was not significant (Table 2 ). These findings indicate that absorption was faster in hypercalciuric patients; however, both patient groups reached similar maximal absorption values. The values of FE and CRE were significantly greater in hypercalciuric patients (Table 2 ), suggesting low ion reabsorption in the kidney tubules.



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  		Figure 1. Concentration–time curves of serum Sr2+ after an oral load in hypercalciuric ({circ}) and normocalciuric ({bullet}) Ca2+ stone formers.

Curves were significantly different (ANOVA for repeated measures; P <0.005). Serum Sr2+ concentrations were increased in hypercalciuric patients 30 and 60 min after the oral load (Mann–Whitney U-test; P <0.05).


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  		Table 2. Results of Sr2+ oral load test in normocalciuric and hypercalciuric stone formers.

In hypercalciuric patients, FE was positively correlated with AUC30 (r = 0.356; P <0.001), AUC60 (r = 0.432; P <0.001), and AUC240 (r = 0.472; P <0.001). The 24-h Ca2+ urine excretion was positively correlated with AUC60 (r = 0.237; P <0.05), but not with the AUC30, AUC240, CRE, or FE. A negative correlation was found between CRE and patient age (r = -0.361; P <0.001). No other correlations were observed in hypercalciuric subjects (Table 3 ).


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  		Table 3. Significant correlation coefficients between AUCs or CRF and the indices of Ca2+metabolism.

All these correlations were not detected in normocalciuric patients, where other kinds of relationships were observed. AUC values correlated with calciotropic hormones plasma concentrations: PTH was negatively correlated with AUC30 (r = -0.383; P <0.005), AUC60 (r = -0.384; P <0.005), AUC240 (r = -0.367; P <0.01), FE (r = -0.410; P <0.005) and CRE (r = -0.318; P <0.05). The calculated values of 1,25(OH)2D3/PTH were positively correlated with AUC30 (n = 27; r = 0.429; P <0.05), AUC60 (n = 27; r = 0.413; P <0.05), and FE (n = 27; r = 0.438; P <0.05), but not with AUC240 or CRE (Table 3Up ).

In both patient groups, CRE did not correlate with the AUCs, and BMD was not related with test results.

When all patients were considered as a whole, the Ca2+ urine excretion was positively correlated with AUC30 (r = 0.244; P <0.005), AUC60 (r = 0.284; P <0.001), AUC240 (r = 0.216; P <0.01), and CRE (r = 0.205; P <0.05); FE was correlated with AUC30 (r = 0.352; P <0.001), AUC60 (r = 0.423; P <0.001), and AUC240 (r = 0.453; P <0.001; Fig. 2 ). CRE was negatively correlated with plasma concentrations of 1,25(OH)2D3 (r = -0.283; P <0.05).



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  		Figure 2. Correlation between urinary Sr2+ FE and enteral Sr2+ absorption 240 min after the oral load, considering all hypercalciuric ({circ}) and normocalciuric ({bullet}) patients.

Sr2+ FE was expressed as percentage of administered oral Sr2+ load, excreted in 4-h urine collected after the Sr2+ assumption. Enteral Sr2+ absorption was expressed as areas under the serum Sr2+ concentration–time curve; n = 140; r = 0.453; P <0.001.


   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
The present work evaluates Ca2+ absorption and renal excretion in hypercalciuric stone formers, using stable Sr2+ as a marker. Results in the control group of normocalciuric stone formers suggest that Sr2+ intestinal absorption is modulated by calciotropic hormones because it was negatively correlated with plasma PTH and positively correlated with plasma 1,25(OH)2D3 normalized to PTH concentrations (15)(16)(17)(18). Accordingly, the negative correlation between CRE and plasma PTH in normocalciuric subjects suggests that tubular Sr2+ reabsorption also is regulated by PTH (15). These correlations were not observed in hypercalciuric patients, who had increased mean values of Sr2+ absorption and renal clearance, in agreement with our knowledge of Ca2+ metabolism in idiopathic hypercalciuria (4)(5)(6)(7)(19)(20). In addition, although Sr2+ clearance was independent of intestinal absorption in both stone-former groups, the correlation between intestinal Sr2+ absorption and FE suggests that in hypercalciuric patients, Sr2+ excretion is strictly linked to the amount of absorbed ions. This link is also confirmed by the correlation between Sr2+ absorption and Ca2+ excretion, which was not observed in normocalciuric patients. These findings are in agreement with the hypothesis of increased body Ca2+ turnover in hypercalciuric patients (20).

The kinetic analysis of the orally administered Sr2+ recognizes two different sites for enteral absorption during the Sr2+ absorption test: the first located in the duodenum, the second located in the jejunum and the initial ileum segment (13)(17)(21). Duodenal absorption is mostly active because of the presence of a pump characterized by high affinity for Ca2+ ions and situated in the enterocyte basolateral plasma membrane (22). Distally to the duodenum, Ca2+ absorption is mostly sustained by nonactive systems, which are less efficient than duodenal mechanisms (22). The significant increase of ion absorption observed 30 and 60 min after the oral load indicates that the most remarkable alteration in hypercalciuric patients concerns the velocity of Ca2+ absorption in the duodenum. It could be caused by the increase of the high-affinity Ca2+ pump activity in enterocytes. The defect of this carrier was observed in erythrocytes from patients with idiopathic hypercalciuria where membrane (Ca2+-Mg2+)ATPase activity was increased (1). Alternatively, these results could be explained by faster gastric emptying, but no data showing a disorder of gastric motility in hypercalciuric patients are available. The lack of a significant difference after 240 min suggests that distally to the duodenum, Ca2+ absorption is similar in hypercalciuric and normocalciuric patients. However, difficulties in finding absorption differences may be attributed to the shortness of the explored enteral segment, to the low efficiency of postduodenal transport systems, and to the underestimation of Ca2+ absorption when Sr2+ is used.

Although the high CRE and excretion reflect the reduction of tubular Ca2+ reabsorption in hypercalciuric patients, renal Sr2+ excretion was correlated with 24-h urinary Ca2+ excretion only when both groups of stone formers were considered. This indicates that estimates of CRE based on the 4-h observation period are not good indicators of tubular Ca2+ handling. The reasons for this inadequacy may be the short period of urine collection during the test (17)(23); the low efficiency of Sr2+ tubular reabsorption, which leads to overestimation of Ca2+ excretion (11)(12); and the binding of Sr2+ ions to plasma proteins, which affects the fraction of filtered ions and renal clearance calculation. In addition, some unknown differences in tubular handling of the two ions may exist. However, it must be pointed out that previous experiences, which showed that Ca2+ excretion in 24-h urine and after an oral load were not correlated (24), indicate that the capacity to excrete an acute ion load may not depend on factors involved in the 24-h urinary Ca2+ excretion and would not necessarily be related to the amount of ions excreted in 24-h urine.

In conclusion, the results of the oral Sr2+ load test suggest that Ca2+ absorption is increased in the duodenum of idiopathic hypercalciuric bone formers. The results also suggest that 4-h CRE can not give a careful assessment of the Ca2+ tubular handling. Finally, in hypercalciuric patients, the physiological control exerted by calciotropic hormones on tubular and enteral transport of Ca2+ ions, which is evidenced in normocalciuric patients, appears to be lost.


   Acknowledgments
 
This work was supported by grants from the Italian Ministry of University and Scientific Research and from the San Raffaele Scientific Institute. We thank Renato Spaventa for helpful criticism and linguistic advice.


   Footnotes
 
Divisions of 1 Nephrology, Dialysis and Hypertension, 2 Urology, and 3 Orthopedics, and 4 Statistics Laboratory, San Raffaele Scientific Institute, 20132 Milan Italy.

1 Nonstandard abbreviations: 1,25(OH)2D3, 1,25-dihydroxyvitamin D; PTH, parathyroid hormone; CRE, Sr2+ renal clearance; BMD, bone mineral density; FE, urine fractional excretion of administered Sr2+; and AUC, area under the plasma Sr2+ concentration–time curve.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Bianchi G, Vezzoli G, Cusi D, Cova T, Elli A, Soldati L, et al. Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria. N Engl J Med 1988;319:897-901. [Abstract]
  2. Weisinger JR. New insights into the pathogenesis of idiopathic hypercalciuria: the role of bone. Kidney Int 1996;49:1507-1518. [Web of Science][Medline] [Order article via Infotrieve]
  3. Nicolaidou P, Themeli S, Karpathios T, Georgouli H, Athanassaki K, Xaidara A, Messaritakis J. Family pattern of idiopathic hypercalciuria and its subtypes. J Urol 1996;155:1042-1044. [Web of Science][Medline] [Order article via Infotrieve]
  4. Lemann J. Calcium and phosphate metabolism: an overview in health and in calcium stone formers. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney stones, medical and surgical management, 1st ed. Philadelphia, PA, Lippincott-Raven, 1996:259–88..
  5. Zerwekh JE, Hughes MR, Reed BY, Breslau NA, Heller HJ, Lemke M, et al. Evidence for normal vitamin D receptor messenger ribonucleic acid and genotype in absorptive hypercalciuria. J Clin Endocrinol Metab 1995;80:2960-2965. [Abstract/Free Full Text]
  6. Shen FH, Baylink DJ, Nielsen RL, Sherrard DJ, Ivey JL, Haussler MR. Increased serum 1,25-dihydroxyvitamin D in idiopathic hypercalciuria. J Lab Clin Med 1977;90:955-962. [Web of Science][Medline] [Order article via Infotrieve]
  7. Broadus AE, Insogna KL, Lang R, Ellison AF, Dreyer BE. Evidence for disordered control of 1,25-dihydroxyvitamin D production in absorptive hypercalciuria. N Engl J Med 1984;311:73-80. [Abstract]
  8. Li XQ, Trembe V, Horovitz GM, Bushinsky DA, Favus MJ. Increased intestinal vitamin D receptor in genetic hypercalciuric rats: a cause of intestinal calcium hyperabsorption. J Clin Investig 1993;91:661-667.
  9. Varecka L, Carafoli E. Vanadate-induced movements of Ca and K in human red blood cells. J Biol Chem 1982;257:7414-7421. [Abstract/Free Full Text]
  10. Vezzoli G, Reina MC, Zerbi S, Spaventa R, Soldati L, Cusi D, Bianchi G. (Ca+Mg)ATPase and calcium influx in erythrocytes of patients with idiopathic hypercalciuria. Biochem Biophys Res Commun 1995;217:1099-1104. [Web of Science][Medline] [Order article via Infotrieve]
  11. Spencer H, Laszlo D, Brother M. Strontium85, calcium45 metabolism in man. J Clin Investig 1957;36:680-687.
  12. Comar CL, Wasserman RH, Ullberg S, Andrews GA. Strontium metabolism and strontium-calcium discrimination in man. Proc Soc Exp Biol Med 1957;95:386-391.
  13. Leeuwenkamp OR, Van der Vijgh WJ, Husken BC, Lips P, Netelenbos JC. Human pharmacokinetics of orally administered strontium. Calcif Tissue Int 1990;47:136-141. [Web of Science][Medline] [Order article via Infotrieve]
  14. Milsom S, Ibbertson K, Hannan S, Shaw D, Pybus J. Simple test of intestinal calcium absorption measured by stable strontium. Br Med J 1987;295:231-234.
  15. Vezzoli G, Baragetti I, Zerbi S, Caumo A, Soldati L, Bellinzoni A, et al. Strontium absorption and excretion in normocalciuric subjects: relation to calcium metabolism. Clin Chem 1998;44:586-590. [Abstract/Free Full Text]
  16. Vezzoli G, Parenti M, Elli A, Corghi E, Costantino A, Saruggia M, et al. Utilizzo di un nuovo test per lo studio dell'assorbimento intestinale del calcio nella IRC. DiPaolo N eds. Nefrologia 1990:1197-1200 Wichtig Publisher dialisi trapianto. Milan. .
  17. Sips AJ, Barto R, Netelenbos JC, Van der Vijgh WJ. Preclinical screening of the applicability of strontium as a marker for intestinal calcium absorption. Am J Physiol 1997;272:E422-E428. [Abstract/Free Full Text]
  18. Molteni N, Bardella MT, Vezzoli G, Pozzoli E, Bianchi P. Intestinal calcium absorption as shown by stable strontium test in celiac disease before and after gluten-free diet. Am J Gastroenterol 1995;90:2025-2028. [Web of Science][Medline] [Order article via Infotrieve]
  19. Hess B, Ackermann D, Essig M, Takkinen R, Jaeger P. Renal mass and serum calcitriol in male idiopathic calcium renal stone formers: role of protein intake. J Clin Endocrinol Metab 1995;80:1916-1921. [Abstract]
  20. Liberman UA, Sperling O, Atsmon Frank M, Modan M, DeVries A. Metabolic and calcium kinetic studies in idiopathic hypercalciuria. J Clin Investig 1968;47:2580-2590. [Medline] [Order article via Infotrieve]
  21. Sips AJ, Van der Vijgh WJ, Barto R, Netelenbos JC. Intestinal absorption of strontium chloride in healthy volunteers: pharmacokinetics and reproducibility. Br J Clin Pharmacol 1996;41:543-549. [Web of Science][Medline] [Order article via Infotrieve]
  22. Kayne LH, Koteva A, Campbell AW, Lee DB. Intestinal absorption of calcium. Massry SG Glassock RJ eds. Textbook of nephrology 3rd ed. 1995:327-339 Williams and Wilkins Baltimore, MD. .
  23. Moraes MEA, Aronson JK. Grahame Smith DG. Intravenous strontium gluconate as a kinetic marker for calcium in healthy volunteers. Br J Clin Pharmacol 1991;31:423-427. [Web of Science][Medline] [Order article via Infotrieve]
  24. Pak CY, Kaplan R, Bone H, Townsend J, Waters O. A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias. N Engl J Med 1975;292:497-500. [Abstract]



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