ABSTRACT
Hyperphosphatemia is recognized as a risk factor for mortality in chronic kidney disease [1]. In addition, serum phosphate concentration within the upper limits of normal is associated with a greater prevalence of vascular and valvular calcification in patients with moderate chronic kidney disease [2]. In the last years, our research group performed human studies involving calcium phosphate supplementation [3-5]. Most studies with calcium phosphate focus on the beneficial effects relating to intestinal metabolism, e.g. bile acid metabolism, fatty acid excretion, and modulation of the microbiota [5-8]. This is because amorphous calcium phosphate is formed in the human gut and, moreover, is able to precipitate intestinal substances, such as bile or fatty acids [6,7,9]. However, calcium phosphate is poorly absorbed in the gut. Evidence comes from studies showing unchanged fasting plasma concentrations of calcium and phosphate after calcium phosphate supplementation [4]. Nevertheless, measuring fasting
concentrations is not a convincing method to examine the influence of calcium phosphate supplementation on calcium and phosphate status. Furthermore, Heaney et al. showed that solubility of a calcium supplement has very little influence on its absorbability and that absorption of calcium from food sources is determined mainly by other food components [10]. In addition, it is necessary to test every calcium product for absorbability [11]. Therefore, in this human study, we examined the postprandial calcium and phosphate concentrations after calcium phosphate supplementation of both a single dose and after three weeks.
