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 343 records · Page 19Linked to original sources
PubMed1992

Citrate and recurrent idiopathic calcium urolithiasis. A longitudinal pilot study on the metabolic effects of oral potassium sodium citrate administered as short-, medium- and long-term to male stone patients.

In male patients with idiopathic recurrent calcium urolithiasis (RCU) the effects of oral potassium sodium citrate (PSC) on acid-base, citrate and mineral metabolism were investigated. There were 17 normocitraturic and 15 hypocitraturic patients. The examination time points in our clinical laboratory were prior to medication and after 3, 6 and over 12 months of medication. Urine collection periods were over 24 h, 2 h--after an overnight fast--3 h postprandially. Acceptance by the patients was poor, a large number refusing to take PSC for 12 months. Compliance of the patients continuing with the study was adequate as assessed by the urinary excretion of potassium and sodium. No unwanted side effects were observed. After 3 months of PSC medication a compensated metabolic alkalosis developed; in the urine calcium was decreased, while citrate, pH and oxalate were increased, as were hydroxyapatite supersaturation and calcium phosphate particles. After more than 12 months of PSC medication, citrate and pH tended toward the pretreatment baseline values, while hydroxyapatite supersaturation and calcium had already returned to pretreatment values. Despite ongoing PSC intake, patients with pre-existing hypocitraturia had lower urinary citrate than patients with previous normocitraturia, while the concomitant pH and hydroxyapatite supersaturation in the urine of the former remained at levels close to those of the latter. Under the influence of PSC, parathyroid gland function remained unchanged, but serum levels of bone alkaline phosphatase and osteocalcin were low, and urinary hydroxyproline was high.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1995

[Citrate and ionized calcium on extracorporeal circulation in pediatric cardiac surgery].

The control of optimum concentrations of ionized calcium Ca2+ during cardiopulmonary bypass is important in maintaining cardiac function and reducing reperfusion injury. Ca2+ may be in part dependent upon the serum level of citrate Cit in use of hemodiluted prime in pediatric cardiac surgery. The purpose of this study was to ascertain fluctuations of Ca2+ during bypass in relation to Cit and to study control of optimum Ca2+. Ca2+ and Cit was measured prior to and every 10 or 20 minutes during bypass in 12 children aged 21 days to 6 years. Of 6 patients (body weight less than 6 kg) received acid-citrate-dextrose (ACD) solution 20 ml before aortic declamp to give low Ca2+ for reducing reperfusion injury. Ca2+ showed initial drop and then gradually increased as the result of decreasing Cit. Ca2+ was inversely correlated with Cit (r = 0.85, p = 0.0001). When ACD 20 ml was added, Ca2+ significantly decreased from 1.00 +/- 0.13 to 0.65 +/- 0.13 mmol/l. However, Cit remained 24.3 +/- 13.3 mg/dl at the end of bypass. In conclusion, the results of this study suggest that gradually increasing Ca2+ during bypass may be related to the rate of citrate metabolism and the use of citrate for the control of Ca2+ remains questionable.

Calcium↗
PubMed1992

Low urine citrate excretion as main risk factor for recurrent calcium oxalate nephrolithiasis in males.

To better define the relative role of metabolic factors in the recurrence of stone formation, we studied the 24-hour urinary excretion of calcium (uCa), citrate (uCit), oxalic acid (uOx) and uric acid (uUa) in 73 male patients with primary calcium oxalate urolithiasis. According to the episodes of stone formation per year, we identified 51 recurrent stone formers (RSF) and 22 single stone formers (SSF). 20 normal adult males constituted the control group (C). uCa and uOx were higher in RSF than in C, but quite similar in SSF and RSF. The only difference between RSF and SSF was uCit, significantly lower (2.06 +/- 1.04 mmol/24 h) in RSF than in SSF (3.22 +/- 1.18 mmol/24 h, p less than 0.001) and in C (3.42 +/- 1.33 mmol/24 h, p less than 0.001). Hypocitraturia (uCit less than 1.5 mmol/24 h) was found in 16 of 51 RSF (31.4%) and in 1 of 22 SSF (4.5%). These data confirm that high levels of uCa and uOx represent a risk factor for lithogenesis, but also strongly indicate the low uCit excretion as the most important urinary abnormality accounting for the recurrence of calcium oxalate stones.

Adult↗
PubMed1993

Effects of citrate on the different phases of calcium oxalate crystallization.

Urinary citrate appears to be an important factor in the crystallization process of calcium oxalate and calcium phosphate. The urinary excretion of citrate was found to be significantly lower in patients with calcium oxalate stone disease as compared with normal subjects, and about 30 per cent of the calcium stone formers can be considered as hypocitraturic. The lowest excretion of citrate was recorded in urine collected during the night. Citrate has significant effects on supersaturation with respect to both calcium oxalate and calcium phosphate, it also inhibits the growth of these crystals. In addition, citrate appears to be capable of inhibiting the aggregation of crystals composed of calcium oxalate, brushite, and hydroxyapatite. The heterogenous growth of calcium oxalate on calcium phosphate is also counteracted by citrate. As a consequence of the crucial role of citrate in these processes, stone prevention with alkaline citrate has become an attractive form of treatment in patients with recurrent stone formation. Single evening dose administration of sodium potassium citrate resulted in an of sodium potassium citrate resulted in an increased excretion of citrate, reduced levels of the calcium/citrate ratio as well as supersaturation with respect to calcium oxalate and a decreased rate of stone formation. However, conflicting results of stone preventive treatment with alkaline citrate have been reported by different groups, and long-term follow-up of patients treated in a randomized way is necessary to definitely assess the efficacy of alkaline citrate.

Calcium Oxalate↗
PubMedDate not supplied

Plasma levels of ionized and total calcium during storage of citrated platelet concentrate.

Measurements of ionized and total calcium levels in supernatant plasma samples from citrated platelet concentrates (PCs) were made over 7 days of storage. Both ionized and total calcium increased significantly during the storage period: respectively, from 0.074 mM Ca2+ in fresh platelet-rich plasma to 0.084 mM in PCs stored for 7 days (p = 0.017), and from 1.94 mM total calcium to 2.06 mM (p = 0.014) over the same period. The increase in calcium was partially blocked by the addition of platelet activation inhibitors to the PCs. Platelet-poor plasma stored under similar conditions showed no significant change in ionized or total calcium, which indicated that the increases observed in PCs were due to the release of cellular calcium. Significant correlations (p less than 0.01) were found between ionized or total calcium levels and lactate concentration or pH, but not hypotonic shock recovery rate. The demonstration of non-zero levels of ionized calcium makes it likely that Ca2+-dependent enzyme systems such as calpain expression and thrombin generation are active in the plasma of citrated PCs and may contribute to the platelet storage lesion.

Alprostadil↗
PubMed1992

Citrate and recurrent idiopathic calcium urolithiasis. A longitudinal pilot study on the metabolic effects of oral potassium citrate administered over the short-, medium- and long-term medication of male stone patients.

In idiopathic recurrent calcium urolithiasis (RCU) in men (n = 37) the metabolic effects of oral tripotassium citrate (PC) were investigated in a longitudinal field study. The patients were either normo- (n = 22) or hypocitraturic (n = 15). Laboratory examinations were performed before, and after 3, 6, and more than 12 months of medication. Acceptance of PC was poor, mainly because of the salty taste of the tablet preparation chosen, and a number of participants dropped out of the study. In the remaining participants, compliance was acceptable when evaluated on the basis of urinary potassium and undesired side effects did not occur. In the short term (up to 3 months), PC evoked compensated metabolic alkalosis (pH and citrate in urine increased; blood gases remained normal), a drop in urinary calcium, together with increasing oxaluria, hydroxyapatite supersaturation, and calcium phosphate crystalluria. In the long term (greater than 12 months) PC urinary pH and citrate "dissociated", in that pH returned to pretreatment baseline values, whereas citrate stayed at high levels. In normocitraturics but not in hypocitraturics, urinary urea and sodium increased with PC. Hypocitraturics appeared to be less sensitive to the effects of PC, as reflected by the relatively small rise in urinary pH and citrate, and they maintained higher mean levels of indicators of bone metabolism (osteocalcin, alkaline phosphatase, hydroxyproline) despite continuous administration of PC. It was concluded that although the PC tablet preparation was effective it may not be an ideal anti-stone drug treatment in the long term and that, especially in hypocitraturics, the intrinsic metabolic defect of RCU may not be sufficiently well controlled.

Acid-Base Equilibrium↗
PubMed1983

Urinary excretion of calcium, magnesium, oxalate and citrate in duodenal ulcer patients. Preliminary results before and up to five years after highly selective vagotomy.

The urinary excretion of calcium, oxalate, citrate and magnesium, and the relative saturation products in urine of either calcium oxalate or calcium phosphate, were determined in male duodenal ulcer (DU) patients preoperatively (n = 60), and 1 and 5 years following highly selective vagotomy (HSV), and in male healthy controls (n = 30). In DU before HSV citrate and magnesium were lowered, oxalate was in the low normal range and calcium was normal. The calcium oxalate product was lower than in controls, while the calcium phosphate product was unchanged. Within 5 years HSV normalized urinary citrate and oxalate, but not urinary magnesium, and the median urinary pH was lower than pre-operatively. There thus results a normal product for calcium oxalate, but a reduced one for calcium phosphate. It is suggested that: (1) unoperated DU patients have a urine composition similar to that exhibited in normocalciuric recurrent calcium urolithiasis; (2) this spectrum of urinary constituents may be changed by HSV.

Adult↗
PubMed1994

Effect of added citrate or malate on calcium absorption from calcium-fortified orange juice.

OBJECTIVE: Calcium absorption was determined from calcium-fortified diluted orange juice, which contained additional citrate or malate, in 16 normal subjects. METHODS: Each load of fortified orange juice with additional citrate (OJ+C) contained 300 mg Ca, 5.7 mEq malate, and 33.6 mEq citrate (10.4 mEq of which were added). Each load of orange juice with additional malate (OJ+M) had 300 mg Ca, 23.2 mEq citrate and 16.1 mEq malate (10.4 mEq of which were added). For each subject, fractional (intestinal) calcium absorption was measured by taking the ratio of fractional forearm radioactivity following an oral administration of OJ+C or OJ+M (labeled with 47Ca) and the fractional forearm radioactivity obtained after intravenous administration of trace 47Ca chloride on a separate occasion. RESULTS: There was no significant difference in fractional calcium absorption from the two calcium-fortified orange juice preparations (40.1 +/- 8.3% for OJ+C and 40.6 +/- 8.6% for OJ+M, p = 0.81). CONCLUSION: Calcium-fortified orange juice with additional citrate provides equivalent bioavailable calcium as the juice with additional malate.

Administration, Oral↗
PubMed1984

Use of potassium citrate as potassium supplement during thiazide therapy of calcium nephrolithiasis.

The effectiveness of potassium citrate as a potassium supplement was compared to that of potassium chloride in 13 patients with calcium nephrolithiasis treated with thiazide. Thiazide treatment alone reduced serum potassium, urinary calcium and citrate without affecting urinary pH. Urinary saturation of calcium oxalate and brushite decreased but not as much as the decrement in urinary calcium because of reduced citrate-calcium complexation. Potassium chloride supplementation averted thiazide-induced hypokalemia and hypocitraturia without influencing hypocalciuric action of thiazide or urinary pH. The decline in urinary saturation of calcium salts paralleled the decrement in urinary calcium. Potassium citrate supplementation also kept urinary calcium low and corrected hypokalemia. Moreover, it increased urinary pH and citrate above levels in other phases. Thus, the ability of thiazide to lower the urinary saturation of calcium oxalate was accentuated by potassium citrate supplementation but not by potassium chloride supplementation, probably owing to increased citrate complexation of calcium. Moreover, the potassium citrate therapy was more effective than potassium chloride supplementation in reducing the propensity for the spontaneous precipitation of calcium oxalate in urine. In conclusion, potassium citrate supplementation may be superior to potassium chloride supplementation in patients receiving thiazide in whom stones form.

Adult↗
PubMed2007

Effect of modification of hydroxyapatite/collagen composites with sodium citrate, phosphoserine, phosphoserine/RGD-peptide and calcium carbonate on bone remodelling.

This study describes the early interface reaction of cancellous bone to a nanocrystalline hydroxyapatite cement containing type I collagen (HA/Coll) and its modifications with sodium citrate (CI), calcium carbonate (CA), phosphoserine (P) and phosphoserine plus RGD-peptide (RGD). Cylindrical implants of HA/Coll and its modifications were inserted into the tibia of Wistar rats. We analysed 6 specimens per group at days 2, 4, 7, 14 and 28. CI, P and RGD modifications showed improved material properties (finer microstructure and higher compressive strength) compared to CA and HA/Coll implants. The powder X-ray diffraction (XRD) showed that the addition of P and CI led to an increase of alpha-TCP peaks while the diffraction patterns of the non-modified cement (HA/Coll) were quite similar with that of natural bone. All of the implants healed without adverse reactions. A significantly higher number of TRAP-positive osteoclasts were observed around CI, RGD and P on day 7 compared to CA and HA/Coll. Around CI, P and RGD a significantly delayed increase of ED1-positive mononuclear cells was detected. The amount of direct bone contact after 28 days was significantly higher around CI, P and RGD compared to CA and HA/Coll implants. The addition of CI, P and RGD appears to enhance bone remodelling at the early stages of bone healing, leading to increased bone formation around HA/Coll composite cements.

Animals↗
PubMed1994

[In vitro effect of citrate and phosphates on calcium transport in the rat ileum].

OBJECTIVES AND METHODS: The effect of the presence of phosphates or citrate on ileal calcium (Ca) absorption was studied by using rat ileum mounted in a Ussing chamber. RESULTS: Mucosa-to-serosa and serosa-to-mucosa undirectional fluxes were not modified by mucosal addition of 2.8 mM Na phosphate or 2.0 mM Na citrate to Krebs-Ringer-bicarbonate buffer containing 1.25 mM CaCl2. However, 50 mM Na citrate induced a significant and similar increase of both unidirectional Ca fluxes, leading to no modification of net Ca flux. This high citrate concentration was associated with a significant increase of tissue conductance and no alteration of zona adherens and tight junction as observed by electron microscopy. CONCLUSIONS: Thus in the absence of any Ca gradient along the epithelium, even at high concentration, citrate did not induced modification of ileal Ca absorption.

Animals↗
PubMed2002

Dosage of potassium citrate in the correction of urinary abnormalities in pediatric distal renal tubular acidosis patients.

Potassium citrate is an alkaline agent that has been recommended for the prevention of nephrolithiasis in distal renal tubular acidosis (RTA). Information on the effectiveness and the optimal dose of potassium citrate in the correction of urinary abnormalities in pediatric distal RTA is limited, however. We conducted this study to determine the effectiveness and the optimal dose of potassium citrate for the correction of urinary abnormalities and the prevention of nephrolithiasis in children with distal RTA. Eight pediatric distal RTA patients participated in this study. The mean +/- SEM age was 9.7 +/- 1.2 years, and mean body weight was 29.1 +/- 4.7 kg. After initial evaluation, all patients were treated with increasing dosages of potassium citrate starting from 2 mEq/kg/d in three divided doses. The dosage was increased progressively in a stepwise fashion every 2 months from 2 mEq/kg/d to 3 mEq/kg/d, then to 4 mEq/kg/d. Blood and 8-hour overnight urine samples were obtained at baseline and every 2 months before increasing the dosage of potassium citrate. Urinary saturations for calcium oxalate and calcium phosphate were estimated by using Tiselius's indices. The basal urinary calcium-to-creatinine, phosphate-to-creatinine, and calcium-to-citrate ratios and urinary saturation for calcium oxalate and calcium phosphate were elevated significantly, whereas citrate-to-creatinine ratio was reduced significantly in distal RTA patients. These ratios were normalized gradually with the increasing dosage of potassium citrate. All the aforementioned abnormalities were normalized only after the dosage of potassium citrate was raised to 4 mEq/kg/d. The elevation in urinary saturation of calcium phosphate could not be normalized throughout the study, however. These results suggest that 4 mEq/kg/d of potassium citrate supplement can correct successfully most of the urinary abnormalities and the elevated urinary saturation for calcium oxalate but not for calcium phosphate in children with distal RTA. Monitoring of urinary calcium-to-creatinine ratio or citrate-to-creatinine ratio is valuable to ensure adequate potassium citrate supplementation in this group of patients.

Acidosis, Renal Tubular↗