Chronic kidney disease (CKD) patients are given calcium carbonate to bind dietary phosphorus and reduce phosphorus retention, and to prevent negative calcium balance. Data are limited on calcium and phosphorus balance in CKD to support this. The aim of this study was to determine calcium and phosphorus balance and calcium kinetics with and without calcium carbonate in CKD patients. Eight stage 3/4 CKD patients, eGFR 36 mL/min, participated in two 3-week balances in a randomized placebo-controlled cross-over study of calcium carbonate (1500 mg/d calcium). Calcium and phosphorus balance were determined on a controlled diet. Oral and intravenous 45calcium with blood sampling and urine and fecal collections were used for calcium kinetics. Fasting blood and urine were collected at baseline and end of each week of each balance period for biochemical analyses. Results showed that patients were in neutral calcium and phosphorus balance while on placebo. Calcium carbonate produced positive calcium balance, did not affect phosphorus balance, and produced only a modest reduction in urine phosphorus excretion compared with placebo. Calcium kinetics demonstrated positive net bone balance but less than overall calcium balance suggesting tissue deposition. Fasting biochemistries of calcium and phosphate homeostasis were unaffected by calcium carbonate. If they can be extrapolated to effects of chronic therapy, these data caution against the use of calcium carbonate as a phosphate binder.

SCF, a nondigestible carbohydrate, increased calcium absorption in free-living adolescent females. Two groups of bacteria may be involved, one directly fermenting SCF and the second fermenting SCF metabolites further, thereby promoting increased calcium absorption. This trial was registered at clinicaltrials.gov as NCT01660503.

Galactooligosaccharides (GOS), prebiotic nondigestible oligosaccharides derived from lactose, have the potential for improving mineral balance and bone properties. This study examined the dose-response effect of GOS supplementation on calcium and magnesium absorption, mineral retention, bone properties, and gut microbiota in growing rats. Seventy-five 4-week-old male Sprague-Dawley rats were randomized into one of five treatment groups (n = 15/group) and fed a diet containing 0, 2, 4, 6, or 8% GOS by weight for 8 weeks. Dietary GOS significantly decreased cecal pH and increased cecal wall weight and content weight in a dose-dependent manner (p < 0.0001). Fingerprint patterns of the 16S rRNA gene PCR-DGGE from fecal DNA indicated the variance of bacterial community structure, which was primarily explained by GOS treatments (p = 0.0001). Quantitative PCR of the samples revealed an increase in the relative proportion of bifidobacteria with GOS (p = 0.0001). Net calcium absorption was increased in a dose-response manner (p < 0.01) with GOS supplementation. Dietary GOS also increased (p < 0.02) net magnesium absorption, femur ⁴⁵Ca uptake, calcium and magnesium retention, and femur and tibia breaking strength. Distal femur total and trabecular volumetric bone mineral density (vBMD) and area and proximal tibia vBMD increased (p < 0.02) with GOS supplementation. Trabecular-rich bones, that is, those that rapidly turn over, were most benefited. Regression modeling showed that GOS benefited calcium and magnesium utilization and vBMD through decreased cecal pH, increased cecal wall and content weight, and increased proportion of bifidobacteria.

Achievement of maximal calcium retention during adolescence may influence the magnitude of peak bone mass and subsequently lower the risk of osteoporosis. Calcium retention is generally considered to reach a plateau at a certain calcium intake. To test this hypothesis, calcium balance was measured in 35 females with a mean (+/-SD) age of 12.7 +/- 1.2 y (range: 12-15 y) who consumed from 841 +/- 153 to 2173 +/- 149 mg Ca/d. Subjects ate a basal diet that included a fortified beverage containing different amounts of calcium citrate malate. Twenty-one subjects were studied at two dietary calcium intakes with use of a crossover design. Results from a previous study in 14 subjects who were studied at only one calcium intake were included in the data analysis. Calcium retention was modeled as a nonlinear function of calcium intake that included a parameter representing mean maximal retention. Mean maximal calcium retention was 473 mg/d (95% CI: 245, 701 mg Ca/d). At higher postmenarcheal ages, maximal calcium retention was lower but the intake required to achieve this was not affected. Calcium intake explained 79% and 6%, respectively, of the variation in fecal and urinary calcium excretion. Intake of 1200 mg Ca/d, the recommended dietary allowance for calcium published in 1989, resulted in a mean calcium retention that was 57% of the maximal value (95% CI: 25%, 89%). Intake of 1300 mg Ca/d was the smallest intake that allowed some adolescent females to achieve 100% of maximal calcium retention (95% CI: 26%, 100%). These data support the idea that calcium retention plateaus at a certain calcium intake although it continues to increase at intakes > 2 g/d.