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PubMed2002

Absorption of calcium fumarate salts is equivalent to other calcium salts when measured in the rat model.

Calcium absorption from fumarate salts (calcium fumarate and calcium malate fumarate), which have recently been considered for use as sources for food and beverage enrichment, was compared to that from calcium citrate malate, calcium citrate, and calcium carbonate. Salts were instrinsically labeled with 45Ca and orally administered to Sprague-Dawley rats. Fractional absorption of calcium from each salt was determined using the femur uptake model. Fractional absorption from the five salts (0.30-0.27) was not significantly different (p > 0.05). Thus, when measured in the rat model, calcium from calcium fumarate and calcium malate fumarate is absorbed equally well as compared to other salts, which are common calcium sources in many foods, beverages, and supplements.

Absorption↗
PubMed1996

Intestinal calcium absorption from different calcium preparations: influence of anion and solubility.

Not only is the calcium content of a preparation significant for providing adequate calcium supplementation for the prophylaxis and therapy of osteoporosis, but also its bioavailability is of essential importance. In the present study, the bioavailability of calcium citrate and calcium lactogluconate/carbonate from a therapeutic dose (= 500 mg Ca2+) was compared in men aged between 45 and 60 years on an intra-individual basis. Calcium citrate was administered both as a solution and as a suspension to 18 healthy volunteers. Using a double-isotope method, the intestinal absorption from the three preparations was determined in randomized order at intervals of 2-4 weeks. The stable isotope 44Ca (20 mg), in highly enriched form, was added in each case to the ready-to-drink solutions and, at the same time, a sterile and pyrogen-free solution containing 5 mg of the stable isotope 42Ca was injected intravenously. The intestinal calcium absorption was then determined after 24 h on the basis of the ratio of the two isotopes in the plasma. There was a significantly higher absorption of 29% from the citrate solution than from the lactogluconate/carbonate solution (25%). Absorption from the citrate suspension was similar to that from the lactogluconate/carbonate solution. While no correlation was found between the measured values for calcium absorption from the three preparations and the plasma concentration of 1,25-dihydroxycholecalciferol, significant inverse correlations with the basal parathyroid hormone concentration were observed for the citrate and lactogluconate/ carbonate solution. The results of this study show that quantitative data on intestinal calcium absorption can be obtained without employing radioactive isotopes in humans. Moreover, they show that calcium absorption is not determined only by the solubility and the degree of ionization of the calcium salt administered, but rather that it is of a complex nature.

Biological Availability↗
PubMed1993

Citrate and calcium effects on Tamm-Horsfall glycoprotein as a modifier of calcium oxalate crystal aggregation.

We measured the effects of Tamm-Horsfall glycoprotein (THP) on calcium oxalate monohydrate (COM) crystal aggregation (Ac) in vitro as well as intrinsic viscosities (Vi) of THP at pH 5.7 and 200 mM NaCl and studied the effects of calcium and citrate on these parameters. THP were isolated from 24-h urines of seven male recurrent calcium stone formers (RCSF) and eight age-matched male healthy volunteers (N, normal). At basal conditions, RCSF-THP inhibited Ac by 28 +/- 10% and normal THP by 60 +/- 6% (P = 0.028). In the presence of calcium, increasing THP concentrations from 16 to 28 and 40 mg/l progressively lowered inhibition by RCSF-THP, but not by N-THP. At 40 mg/l, inhibition by N-THP was 27 +/- 9% vs. -43 +/- 8% by RCSF-THP (P = 0.001), i.e., all stone former THP promoted Ac. With an additional 3.5 mM of citrate, inhibition of Ac was 56 +/- 5% by normal and 34 +/- 6% by stone former THP (P = 0.021), and all seven stone former THP again inhibited Ac. Vi of RCSF-THP was higher than that of N at basal conditions (162 +/- 21 vs. 93 +/- 15 ml/g, P = 0.021) and in the presence of 5 mM calcium (352 +/- 54 vs. 118 +/- 17 ml/g, P = 0.001), i.e., RCSF-THP were more self-aggregated, but not when citrate was added (185 +/- 29 vs. 123 +/- 19 ml/g). (ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1963

URINARY EXCRETION OF CALCIUM AND CITRATE IN NORMAL INDIVIDUALS AND STONE FORMERS WITH VARIATION IN CALCIUM INTAKE.

The changes which occur in both calcium and citrate excretion in normal persons, in idiopathic calcium stone formers and in persons with hyperparathyroidism have been measured at high and low levels of dietary calcium intake. The findings suggested a difference in the renal handling of calcium between normal subjects and stone formers. There was a greater increase in the urinary excretion of calcium with increased intake of calcium in individuals with renal calculi than in normals. Increasing the calcium intake shifted the mole ratio of calcium to citrate unfavourably for the chelation of calcium by citrate, and this unfavourable shift was more marked in the stone formers than in normal individuals. These findings support the concept that urinary citrate may be of importance in the prevention of calcium precipitation and hence in the pathogenesis of kidney stones.

Calcium↗
PubMedDate not supplied

Acute oral calcium-sodium citrate load in healthy males. Effects on acid-base and mineral metabolism, oxalate and other risk factors of stone formation in urine.

The currently preferred calcium preparations for supplementation of food vary widely with respect to calcium availability, effects on systemic mineral metabolism, acid-base status, and the calciuria-induced risk of urinary tract stone formation. In eight healthy males we studied the response to an acute load with alkali(sodium)-containing soluble calcium citrate (CSC) (molar ratio calcium/sodium/citrate approx. = 1/1/1), when taken in three different doses (10, 20, 30 mmol calcium) together with a continental breakfast. Intestinal calcium absorption, serum calcium, calcitonin, parathyroid hormone (PTH) other markers of bone metabolism, net acid excretion and calcium oxalate crystallization in urine were evaluated. CSC evoked a dose-dependent increase in calcium absorption, calcium in serum and urine, but no overt hypercalcemia, and calciuria was low relative to the excess calcium ingested; PTH fell and calcitonin rose (p < 0.05 vs. breakfast alone), but the diet-independent markers of bone resorption declined only insignificantly, while the markers of bone formation and turnover remained unchanged. There was a significant "once-daily" effect (= cumulative 24 h postload response) of CSC: a decrease in urinary cyclic AMP, phosphorus, and ammonium, and an increase in urinary bicarbonate. Soon after CSC intake, urinary calcium oxalate and hydroxyapatite supersaturation increased dose-dependently, the calcium oxalate crystal diameter was increased, but crystal aggregation time, which is crucial for stone formation, remained statistically unchanged. Thus, CSC provides calcium in a bioavailable form, creates mild systemic alkalinisation and inhibition of bone resorption, but leaves the risk of developing urinary stones unchanged. Comparative long-term studies on bone growth and the maintenance of bone health, using alkali-containing versus alkali-free calcium citrate, appear worthwhile.

Administration, Oral↗
PubMed1992

Reduction of urinary oxalate by combined calcium and citrate administration without increase in urinary calcium oxalate stone formers.

Oxalic acid seems to play a far greater role in the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of sodium potassium citrate were administered to 46 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of urinary oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs was discussed.

Adult↗
PubMed1975

[Effects of administering diets with starch or sucrose basis on certain parameters of calcium metabolism in the young, growing rat].

The important role of many carbohydrates on calcium metabolism has been demonstrated by FOURNIER and DUPUIS. Starch, however, neither influences the absorption nor the retention of calcium. Less is known about the effects of sucrose. In this study the influence of starch on calcium metabolsim has been compared with that of sucrose. Male weanling Wistar rats were divided into three groups according to their diets. The first group received a refined and well-balanced diet (except for the absence of vitamin D), containing 68 p. 100 of starch. The second group received the same diet except sucrose was substituted for the starch. The third group received the same diet as Group 1, with the addition of vitamin D. Plasma calcium citrate and urinary citrate and calcium were determined. At the age of 2 months after one night of fasting, each group of rats was injected intraperitoneally with a 1 ml, aqueous solution containing 1 mg calcium and 0, 6 mu Ci45Ca. Twenty-four hours later the animals were sacrificed and the calcium femur percentage, radioactivity p. 1,000 of the injected dose of 45Ca, and specific radioactivity were determined. When performance data from Group 3 were compared to Group 1 and Group 2, the following results were obtained: --Group 1 (starch diet without vitamin D) had very low plasma calcium levels; urinary calcium, plasma citrate and urinary citrate levels were lowered, and the calcium femur percentage was smaller. Bone avidity for calcium was found. --Group 2 (sucrose diet without vitamin D) had normal plasma calcium levels. Urinary calcium and citrate and plasma citrate did not show significant differences from those of animals receiving vitamin D. No significant differences were found in the specific radioactivity and radioactivity p. 1,000 of the administered dose. Contrary to starch, sucrose maintained calcium homeostasis, and apparently, normal ossification, although the femur was lighter than those of animals receiving vitamin D. Further work is necessary to determine whether the fructose component of the sucrose molecule is responsible for the increased calcium utilization and, if so, what levels of ingestion are necessary for this activity.

Animals↗
PubMed1977

The effect of fluorocitrate on urinary calcium and citrate excretion.

The renal handling of calcium and citrate was studied in dogs after the administration of fluorocitrate. The drug produced a significant increase in urinary calcium and citrate excretion. Net renal secretion of citrate occurred during the infusion of fluorocitrate since citrate clearances exceeded the glomerular filtration rate.

Acidosis↗
PubMed1991

Calcium metabolism in acidotic patients induced by carbonic anhydrase inhibitors: responses to citrate.

Calcium metabolism and its response to citrate were examined in 51 patients with glaucoma receiving carbonic anhydrase inhibitors (acetazolamide or methazolamide). Metabolic acidosis, hypocitraturia and increased incidence of nephrolithiasis were induced by both drugs. However, the acidosis was milder with methazolamide administration. Normocalciuria was observed in 29 patients and was shown to be a result of low filtered calcium. Renal hypercalciuria in 16 patients was associated with elevated parathyroid hormone but nephrogenic cyclic adenosine monophosphate remained within normal limits. Citrate in the form of potassium citrate (4.3 mmol.) and sodium citrate (4.0 mmol.) did not correct the metabolic acidosis or hypocitraturia but consistently decreased fasting and 24-hour urinary calcium excretion in patients with renal hypercalciuria. This event did not occur in patients with normocalciuria or absorptive hypercalciuria. These results suggest that a small amount of citrate could reverse renal hypercalciuria without correcting the metabolic acidosis.

Acetazolamide↗
PubMed1999

Acute effects of calcium sodium citrate supplementation of a test meal on mineral homeostasis, oxalate, and calcium oxalate crystallization in the urine of healthy humans--preliminary results in patients with idiopathic calcium urolithiasis.

Calcium, in the form of regular food supplementation, can improve bone metabolism, but it can also increase the risk for renal calcium stones, and may aggravate pre-existing calcium urolithiasis. To study the first of these two aspects, ten healthy volunteers were given a conventional test meal (breakfast; calcium content 28 mg) with or without two dosages of calcium (as calcium-sodium citrate, CSC 1, 680 mg; CSC 2 1,360 mg), taken after an overnight 12 h fast. To study the latter aspect, patients with idiopathic recurrent calcium urolithiasis (ICU) received a balanced test meal of fixed composition, containing 1,000 mg calcium either as CSC (Meal + CSC3; n = 6) or as calcium gluconate (Mcal; n = 8). In normals, CSC induced a dose-dependent increasing intestinal absorption of calcium, and a decrease in oxalate absorption; in serum, CSC increased calcitonin and suppressed parathyroid hormone, but left unchanged the markers of bone turnover, serum osteocalcin and bone alkaline phosphatase. In urine, CSC decreased bone resorption markers (collagen crosslinks) and phosphaturia increased citrate, created signs of metabolic alkalosis, and inhibited several parameters of CaOx crystallization. In ICU, the CSC3 load failed to promote the crystallization of CaOx and calcium phosphate. It was concluded that CSC supplementation of a meal: (1) is well tolerated by healthy subjects and ICU patients, renders calcium highly available to bone, and prevents post-prandial oxaluria from rising; and, (2) is followed by the inhibition of crystallization of renal stone forming calcium-containing substances. Long-term studies aimed at evaluating the usefulness of CSC in preserving healthy bone, and in the metaphylaxis of renal stones would appear justified.

Adult↗
PubMedDate not supplied

Analysis of calcium, oxalate, and citrate interaction in idiopathic calcium urolithiasis in children.

The majority of urinary stones in children are composed of calcium oxalate. To investigate the interaction between urinary calcium, oxalate, and citrate as major risk factors for calcium stones formation, their 24-h urinary excretion was determined in 30 children with urolithiasis and 15 normal healthy children. The cutoff points between children with urolithiasis and healthy children, accuracy, sensitivity, and specificity for each risk factor alone as well as for all three taken together were determined. OneR and J4.8 classifiers as parts of the larger data mining software Weka, based on machine learning algorithms, were used for the determination of the cutoff points for differentiation of the children. The decision tree based on J4.8 classifier analysis of all three risk factors together proved to be the best for differentiating stone formers from normal children. In comparison to the accuracy of the differentiation after calcium and oxalate of 80% and 75.6%, respectively, the decision tree showed an accuracy of 97.8%. Even when its stability was tested by the leave-one-out cross-validation procedure, the accuracy remained at a very acceptable percentage of 93.2% correctly classified patients. J4.8 classifier analysis gave a look inside urinary calcium, oxalate, and citrate interaction. Urinary calcium excretion was shown as the most informative in discrimination of the children with urolithiasis from healthy children. However, it was shown that oxalate and citrate excretions might influence the stone formation in a subpopulation of the stone formers. In patients with low urinary calcium, a major role in lithogenesis belongs to oxalate, in some of them alone and in others in conjunction with citrate. Decreased urinary citrate excretion in the presence of increased oxalate excretion may lead to stone formation.

Adolescent↗
PubMed1994

Inter-relations between the calcium set-points of Parfitt and Brown in primary hyperparathyroidism: a sequential citrate and calcium clamp study.

The objective of the present study was to compare the calcium set-points of E. M. Brown and A. M. Parfitt obtained by sequential citrate and calcium clamp in patients with primary hyperparathyroidism and healthy controls. Twenty-six patients with primary hyperparathyroidism were investigated and compared to 22 healthy volunteers. All participants were investigated by sequential calcium lowering and raising comprising the following four phases: Phase (1) blood ionized calcium lowering of about 0.20 mmol l-1; phase (2) steady-state (relative) hypocalcaemia of blood ionized calcium 0.20 mmol l-1 below baseline; phase (3) blood ionized calcium is raised to about 0.20 mmol l-1 above baseline; and phase (4) (relative) hypercalcaemia of blood ionized calcium 0.20 mmol l-1 above baseline. Serum parathyroid hormone (1-84) was measured by an immunoradiometric assay. Blood ionized calcium was measured by a calcium selective electrode. We found the calcium set-points of Parfitt to be 1.42 mmol l-1 (SD 0.12, n = 52) vs. 1.25 mmol l-1 (SD 0.04, n = 44) in patients and controls, respectively (P < 0.001). The calcium set-points of Brown were 1.32 mmol l-1 (SD 0.10, n = 26) vs. 1.13 mmol l-1 (SD 0.04, n = 22), respectively (P < 0.001). By comparing the calcium set-points of Parfitt and Brown, a strikingly good correlation was observed, in patients (r = 0.91, P < 0.001) and in controls (r = 0.85, P < 0.001). We demonstrate in this paper in vivo that Brown's and Parfitt's calcium set-points are raised in primary hyperparathyroidism and return to normal following parathyroidectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1962

Urinary calculi in germfree rats.

In a colony of germfree rats 50 per cent of the males had urinary calculi composed of calcium citrate and calcium oxalate. Genetically closely related conventional animals on the same sterilized diet did not present a single case of stone formation. The tendency to calculus formation disappeared when germfree animals were contaminated with the intestinal flora from conventional rats. The calculus formation can readily be explained by the high calcium, high citrate, and high pH of the urine. This pattern was changed to that of conventional rats when the germfree rats were infected with intestinal microorganisms.

Animals↗