Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Calcium Citrate”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed1992

Calcium, phosphate and citrate in human milk at initiation of lactation.

The onset of copious milk secretion (lactogenesis II) in women occurs between 1 and 3 d after birth, and during this period the composition of breast milk changes. During the first 5 d of lactation we measured the concentrations of total, diffusible and ionized Ca (Catot, Cad, Ca2+), diffusible phosphate (Pid), diffusible citrate (Citd) and lactose in the breast milk. On day 1 after birth the concentrations (mean +/- SEM) were Catot, 5.71 +/- 0.30 mM; Cad, 2.66 +/- 0.19 mM; Ca2+, 2.90 +/- 0.18 mM; Pid, 0.26 +/- 0.16 mM; Citd, 0.25 +/- 0.03 mM and lactose, 76 +/- 11 mM. Between day 1 and day 4 the concentration of Catot increased 1.7-fold to 9.56 +/- 0.39 mM, Cad increased 1.8-fold to 4.75 +/- 0.26 mM, Ca2+ decreased by 20% to 2.33 +/- 0.13 mM, Pid increased 6.6-fold to 1.69 +/- 0.11 mM, Citd increased 20-fold to 5.06 +/- 0.21 mM, and lactose increased 2.3-fold to 173 +/- 4 mM. A high correlation has been found between [Cad] and [Citd] in the milk of both ruminant and non-ruminant species, which show a wide range in concentrations of [Cad] and [Citd], and the data fit a simple physicochemical model of ion equilibria in the aqueous phase of milk. The results of the present study confirm the relationship between [Cad] and [Citd] in human milk, even during lactogenesis II when the composition of the milk is changing very rapidly.

Adult↗
PubMed1985

[Effect of cocoa on excretion of oxalate, citrate, magnesium and calcium in the urine of children].

Cocoa is a strong carrier of oxalic acid (average: 400 mg per 100 g). In three calcium oxalate stone formers clinical observation had been suggestive of excessive intake of cocoa products contributing to calculus formation. We studied the effect on renal oxalate excretion of an oral cocoa load (30 g per m2 body surface given on 2 consecutive days) in 12 former stone formers (group 1), 14 children with isolated microscopic haematuria (group 2), 13 healthy boys (group 3), and 12 healthy girls (group 4). A new enzymatic method was used to measure oxalic acid in cocoa products as well as in urine samples by a two step reaction: 1. Oxalate decarboxylase, 2. formiate dehydrogenase with photometry of NADH. In addition, the daily excretion of the following substances was measured: Citrate, magnesium, and calcium. There was a significant increase of urinary oxalate excretion from an average of 14.5 mg/24 hours before to an average of 22.2 mg/24 hours after the load in healthy children, and a similar increase in stone formers, but not in children with microscopic haematuria. The excretion of citrate and magnesium did not change following cocoa intake. The calcium excretion was higher in stone formers than in the other groups, but the difference was significant only compared to group 2. It is concluded that the risk of calculus formation may increase following continuous and excessive intake of cocoa products in children with a tendency toward hypercalciuria. Counselling of the stone formers resulted in a marked drop of the daily oxalate excretion, and there was no recurrence of calculus formation over a period of 6 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2005

Effects of potassium alkali and calcium supplementation on bone turnover in postmenopausal women.

Potassium citrate may improve calcium balance by conferring an alkali load. Calcium supplementation slows postmenopausal bone loss by inhibiting PTH secretion. This study explores whether combined treatment with potassium citrate and calcium citrate is more effective than either agent alone in inhibiting bone loss. In a crossover study involving 18 postmenopausal women, the following treatments were compared: potassium citrate (4.3 g or 40 mmol/d), calcium citrate (800 mg or 20 mmol/d), combined treatment, and placebo. During the last 2 d of each 2-wk phase, serum and 24-h urine were collected for assessment of calcium metabolism, alkali load, and bone turnover markers. Compared with placebo, potassium citrate provided an alkali load and significantly decreased urinary calcium without changing serum PTH (sPTH) or bone turnover markers. Calcium citrate significantly increased absorbed calcium, marginally decreased sPTH, and significantly reduced bone resorption markers. Combined treatment retained key features of potassium citrate and calcium citrate. However, more alkali was delivered than with potassium citrate alone, and absorbed calcium did not differ from calcium citrate alone. Compared with placebo, combined treatment increased urinary calcium, marginally reduced sPTH, provided a clear alkali load, and reduced the bone resorption markers serum type I collagen C-telopeptide and urinary N-telopeptide by 20.4% (P < 0.0001) and 18.2% (P = 0.005), respectively. A significant trend was noted for the decrease in bone resorption markers as treatment changed from placebo to potassium citrate to calcium citrate to combined treatment. In postmenopausal women, combined treatment with potassium citrate and calcium citrate inhibits bone resorption by providing an alkali load and increasing absorbed calcium.

Bone Resorption↗
PubMed1979

The effects of citrate and extracellular calcium ions on the platelet release reaction induced by adenosine diphosphate and collagen.

The ADP-induced release of 3H-serotonin from human platelets in heparinized platelets rich plasma is markedly stimulated by the addition of sodium citrate. The aggregation and release that is induced by collagen is less affected by citrate. Data is presented that supports the view that the effects of citrate on both ADP- and collagen-induced release are largely via alteration of the concentration of ionized calcium in plasma. Collagen can induce release of 3H-serotonin via extracellular calcium-independent and -dependent mechanisms. The possibility that the calcium-dependent mechanism is aggregation-dependent and that the calcium is required for platelet aggregation rather than directly involved in the release reaction is discussed.

Adenosine Diphosphate↗
PubMed1995

Intracellular citrate induces regenerative calcium release from sarcoplasmic reticulum in guinea-pig atrial myocytes.

Ca2+ release from the sarcoplasmic reticulum was studied in voltage-clamped guinea-pig atrial myocytes. Cells were dialysed with a pipette solution containing the Ca2+ indicator 1- [2-amino-5-(6-carboxyindol-2-yl) phenoxy]-2-(2'-amino-5'-methylphenoxy) ethane-N,N,N',N'-tetraacetic acid] (Indo-1, 100 microM) and as main anion either chloride or the low-affinity Ca2+ buffer citrate. Intracellular Ca2+ transients (Cai transients) were elicited by depolarizations from a holding potential of -50 mV. In chloride-dialysed cells, Cai transients showed a bell-shaped dependence on the amplitude of the depolarizing pulse. In citrate-dialysed cells, membrane depolarizations were associated with a small rise in [Ca2+]i. These small changes in [Ca2+]i were either followed by a large Cai transient or failed to induce large changes in [Ca2+]i. The peak amplitude of the large Cai transient did not vary with the amplitude of the depolarizing pulse. These results demonstrate that in the presence of intracellular chloride, Ca2+ release in atrial cells is a graded process triggered by Ca2+ influx. Using citrate as the main intracellular anoin, Ca2+ release triggered by Ca2+ entry was no longer graded but occurred in a regenerative manner. The results are discussed in terms of two models in which citrate, affects the spatial distribution of [Ca2+]i or the loading state of the sarcoplasmic reticulum.

Animals↗
PubMed1993

Scanning electron microscopic study of the effect of citrate and pyrophosphate on calcium oxalate crystal morphology.

The effects of citrate and pyrophosphate on the morphology of calcium oxalate monohydrate crystals formed in a supersaturated calcium oxalate solution were examined by scanning electron microscopy. Within the normal range of urinary concentrations, citrate and pyrophosphate affected the morphology of the crystals. The length/width ratio of the crystals decreased at higher concentrations of citrate and pyrophosphate. Citrate seems to have a dual mechanism of inhibition of crystal growth (binding to the crystal surfaces) and of complexation (with calcium in the solution). Pyrophosphate is believed to bind preferentially to calcium in the solid phase rather than in the solution phase, as it affected crystal morphology at very low concentrations and was detected on the crystals by X-ray microanalysis. Pyrophosphate seems to bind to the monohydrate but not to the dihydrate.

Calcium Oxalate↗
PubMed1999

Magnesium, citrate, magnesium citrate and magnesium-alkali citrate as modulators of calcium oxalate crystallization in urine: observations in patients with recurrent idiopathic calcium urolithiasis.

The effects of magnesium (Mg) and citrate on the metastable limit of calcium oxalate (CaOx) solubility (synonym: tolerable oxalate TO) were examined in artificial urine and in postprandial urine of male patients with idiopathic calcium urolithiasis (ICU). In artificial urine increasing pH, Mg and citrate elevate TO, decrease CaOx supersaturation only marginally, but elevate considerably free citrate; the effect of Mg alone was small in comparison with citrate alone, and the effects of both substances appeared additive. In ICU patients, matched for sex, age and CaOx supersaturation to non-stone-forming controls, TO was decreased (mean values 0.33 vs. 0.52 mM/l in controls, P < 0.05). Additional significant (P < 0.05) differences were found between ICU and controls: the former exhibited increased CaOx crystal growth, decreased crystal agglomeration time, a more acidic urinary pH, increased concentrations of free calcium and free Mg, and decreased free oxalate and free citrate. After ingestion of a urine-acidifying test meal, or this meal supplemented with either neutral Mg citrate or Mg-alkali citrate, by three groups of male ICU patients, matched for age and CaOx supersaturation, only the last-named preparation evoked an increase in TO and a decrease in crystal diameter, while the normally occurring pH decline from fasting urine was virtually abolished, and the ratios urinary Mg/citrate and calcium/citrate tended towards low values. In contrast, Mg citrate increased crystal agglomeration time, while changes in the other parameters were only insignificant. The crystals formed in urine were CaOx di- and monohydrate (by electron microscopy), and energy dispersive X-ray analysis showed calcium peaks exclusively. However, chemical analysis of crystals verified the presence not only of oxalate and calcium, but also of Mg, phosphate, citrate, and urate; moreover, these crystal constituents seemed to be influenced by Mg citrate and Mg-alkali citrate in different ways. It was concluded that (1) Mg and citrate are effectors of TO in artificial and natural urine; (2) in ICU, low TO and other disturbed CaOx crystallization parameters appear related to the prevailing low urinary pH and low free citrate; (3) Mg-alkali citrate inhibits CaOx crystallization, probably via actions of the citrate, but not the Mg. Because of the eminent role of Mg in human health and ICU, further studies on crystallization after oral intake of Mg in the form of citrate are warranted.

Calcium Oxalate↗
PubMed1987

Inhibition by citrate of spontaneous precipitation of calcium oxalate in vitro.

Effect of citrate on the spontaneous precipitation of calcium oxalate was examined in synthetic media. Citrate significantly increased the formation product of calcium oxalate. This "direct" measure of inhibitor activity, representing activity product at the point of nucleation, rose by 76% by the addition of citrate sufficient to provide trivalent citrate concentration of 1.49 mM. Moreover, citrate inhibited calcium oxalate crystallization by complexing calcium and lowering calcium oxalate saturation. This "indirect" measure of inhibitor activity was assessed from the concentration product of calcium oxalate at the point of nucleation, since this measure should provide a reflection of both ion pair formation and direct inhibitor activity of citrate. The concentration product exceeded the formation product at all ionic (trivalent) citrate concentrations, particularly at high ionic citrate levels. At the ionic citrate concentration of 1.49 mM, the rise in the concentration product was 373%, which was nearly fivefold that observed for the formation product. The presence of ferric or aluminum cations at a physiologic concentration of 2 mg/l did not modify the increase in formation product produced by citrate. Thus, citrate inhibits calcium oxalate crystallization, largely by complexing citrate, but also by directly affecting nucleation. Presence of ferric or aluminum cations at a physiological concentration does not modify the inhibitor action of citrate.

Calcium Oxalate↗
PubMed1996

Is citrate an inhibitor of calcium oxalate crystal growth in high concentrations of urine?

The effect of citrate on calcium oxalate (CaOx) crystal growth was studied in a system in which series of samples containing [45Ca]calcium chloride were brought to different levels of supersaturation with various concentrations of oxalate. The crystallization was assessed by measuring the amount of isotope remaining in solution 30 min after the addition of CaOx seed crystals to samples containing citrate in concentrations corresponding to those in final urine. The experiments were carried out both in pure salt solutions and in solutions with dialysed urine. Increased concentrations of citrate resulted in a reduced crystallization of CaOx in both the presence and absence of dialysed urine, but with the lowest rate of crystallization in the samples containing urine. The increased concentration of 45Ca remaining in solution reflected a reduced crystallization, which could possibly be explained both by a reduced supersaturation and by an increased inhibition of CaOx crystal growth. The direct effects of citrate on CaOx crystal growth were assessed by calculating the ion-activity product of CaOx (APCaOx) at corresponding degrees of crystallization. The APCaOx recorded at a 30% reduction of the amount of isotope in solution increased with increasing concentrations of citrate between 1.0 and 1.5 mmol/l samples both with and without dialysed urine. These findings indicate that citrate has a weak direct inhibitory effect on CaOx crystal growth, which adds to the reduced growth rate brought about by urinary macromolecules and a decreased supersaturation.

Antacids↗
PubMed2002

Prevention of spinal bone loss by potassium citrate in cases of calcium urolithiasis.

PURPOSE: We determine if potassium citrate treatment stabilizes spinal bone density among patients with recurrent calcium oxalate nephrolithiasis. MATERIALS AND METHODS: We studied a group of 16 men and 5 women with stones taking potassium citrate from 11 to 120 months. They represented all patients from the Stone Clinic who took potassium citrate alone for at least 11 months. L2-L4 bone mineral density data before and after potassium citrate treatment were retrieved retrospectively and analyzed. RESULTS: In the combined group L2-L4 bone mineral density increased significantly by 3.1% over mean duration of 44 months. Z score, corrected for age matched normal values, increased significantly by 3.8%. Urinary pH, citrate and potassium increased significantly during treatment but urinary calcium did not change. CONCLUSIONS: Potassium citrate, a commonly used drug for the prevention of recurrent nephrolithiasis, may avert age dependent bone loss. Spinal bone density increased in most patients when it normally decreases.

Adult↗