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NDT Advance Access originally published online on July 31, 2008
Nephrology Dialysis Transplantation 2008 23(10):3368-3369; doi:10.1093/ndt/gfn428
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Oral calcium load and fractional intestinal calcium absorption

Nephrol Dial Transplant 2008; doi:10.1093/ndt/gfn432

E-mail: drueke{at}necker.fr

Sir,

Heinrich et al. [1] examined the effect of calcium carbonate intake, as compared to that of sevelamer intake, on intestinal calcium absorption and urinary calcium excretion in healthy human volunteers. The authors reason that under steady-state conditions urinary calcium excretion ‘corresponds’ to calcium load in healthy subjects. This statement is correct for adult individuals but only for net calcium absorption from the gut, that is taking into account total intestinal calcium absorption minus calcium entering the gut lumen via intestinal, biliary and pancreatic secretions. The authors claim that by determining urinary excretion of calcium they are able to measure ‘fractional intestinal absorption’ of calcium. We think this claim is incorrect. To determine fractional intestinal absorption one has to use an isotope method, administering either a single calcium isotope [2] or two different calcium isotopes [3] together with ‘cold’ calcium and then calculating fractional absorption based on radioactivity decay in the blood. The best way to determine net absorption is to carry out balance studies. Admittedly, these methods are time and energy consuming.

When Heinrich et al. acutely switch their healthy volunteers from a dietary calcium intake of 36 mmol/day to 76 mmol/day, by adding 40 mmol/day elemental calcium in the form of calcium carbonate, the individuals are no longer in the steady state for at least some days. Following changes in calcium intake, long-term balance studies have shown that a delay of at least 30 days is necessary to reach the steady state [4]. Under non-steady-state conditions, urinary calcium excretion does no more reflect oral calcium intake.

Considering the above two shortcomings, it is not surprising that the estimates of fractional calcium absorption values in their healthy volunteers, in the presence or absence of an additional oral calcium load, namely 8.7–14.8%, are much lower than the values that are generally reported in the literature using validated methods, namely 20–40% [5,6].

Finally, the finding that serum calcium does not change in response to calcium carbonate loading is not unexpected since the organism has invented powerful mechanisms allowing serum ionised calcium to be maintained within narrow limits. The failure to observe a change in serum PTH can be explained by too much delayed blood sampling after the preceding calcium load. Circulating PTH needs to be measured 1–3 h after an oral calcium load in order to observe a transient decrease in hormone concentration. This has again been shown in a recent study in which the authors administered a mixed oral calcium (390 mg) and phosphate (500 mg) load to healthy volunteers and found a slight but significant decrement in serum PTH after 30, 60 and 150 min, but not thereafter [7]. Of interest, they did not observe such an early decrement in patients with chronic renal failure.

In conclusion, taking urinary calcium excretion as a measure of fractional intestinal calcium absorption in healthy subjects is unreliable.

Conflict of interest statement. None declared.

Tilman B. Drüeke1 and Jacques Chanard2

1 Inserm Unit 845 and Division of Nephrology, Necker Hospital, Paris 2 Division of Nephrology CHU Reims, Reims France

References

  1. Heinrich T, Heidt H, Hafner V, et al. Calcium load during administration of calcium carbonate or sevelamer in individuals with normal renal function. Nephrol Dial Transplant (2008).
  2. Chanard JM, Drueke T, Zingraff J, et al. Effects of haemodialysis on fractional intestinal absorption of calcium in uraemia. Eur J Clin Invest (1976) 6:261–264.[CrossRef][Web of Science][Medline]
  3. Heaney RP, Saville PD, Recker RR. Calcium absorption as a function of calcium intake. J Lab Clin Med (1975) 85:881–890.[Web of Science][Medline]
  4. Birge SJ, Peck WA, Berman M, et al. Study of calcium absorption in man: a kinetic analysis and physiologic model. J Clin Invest (1969) 48:1705–1713.[Web of Science][Medline]
  5. Bronner F. Nutrient bioavailability, with special reference to calcium. J Nutr (1993) 123:797–802.[Abstract/Free Full Text]
  6. Heaney RP. Quantifying human calcium absorption using pharmacokinetic methods. J Nutr (2003) 133:1224–1226.[Abstract/Free Full Text]
  7. Isakova T, Gutierrez O, Shah A, et al. Postprandial mineral metabolism and secondary hyperparathyroidism in early CKD. J Am Soc Nephrol (2008) 19:615–623.[Abstract/Free Full Text]

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