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 217 records · Page 12Linked to original sources
PubMed1996

The effect of a short course of calcium and vitamin D on bone turnover in older women.

Calcium and vitamin D (1200 mg/day + 800 IU) has been shown to reduce hip fracture incidence in older women living in long-term care facilities who had borderline low vitamin D levels. We examined the effect of a short course of calcium and vitamin D on biochemical markers of bone turnover in older community-living women. Twelve community-living women (mean age 75 years) in good general health, without diseases or on medications known to affect bone, were entered into the study. All women were treated with calcium citrate (1500 mg/day of elemental calcium) and vitamin D3 (1000 IU/day) (Ca + D) for 6 weeks. Biochemical markers of bone turnover were measured in serum and urine collected at baseline (two samples), 5 and 6 weeks on Ca + D, and 5 and 6 weeks after termination of Ca + D. Markers of bone formation were osteocalcin, bone alkaline phosphatase and type I procollagen peptide. Markers of bone resorption were urinary hydroxyproline, free pyridinoline and deoxypyridinoline crosslinks, and N-telopeptides of type I collagen. Parathyroid hormone (PTH) and 25-hydroxyvitamin D were also measured at baseline, 6 weeks on treatment and 6 weeks after termination of treatment. All markers of bone resorption decreased on Ca + D and returned to baseline after termination of Ca + D (p < 0.05). Markers of bone formation did not change with Ca + D treatment. PTH decreased on Ca + D and returned to baseline after treatment, and 25-hydroxyvitamin D increased with treatment and remained elevated 6 weeks after the end of treatment. We conclude that Ca + D reduces bone resorption in older women, possibly by suppressing PTH levels.

Aged↗
PubMed1985

Effects of chemical speciation on the mineralization of organic compounds by microorganisms.

The mineralization of 1.0 to 100 ng each of four complexing compounds-oxalate, citrate, nitrilotriacetate (NTA), and EDTA-per ml was tested in media prepared in accordance with equilibrium calculations by a computer program so that the H, Ca, Mg, Fe, or Al complex (chemical species) was predominant. Sewage microorganisms mineralized calcium citrate more rapidly than iron, aluminum, or hydrogen citrate, and magnesium citrate was degraded slowest. Aluminum, hydrogen, and iron oxalates were mineralized more rapidly than calcium oxalate, and magnesium oxalate was decomposed slowest. Sewage microorganisms mineralized calcium NTA but not aluminum, magnesium, hydrogen, or iron NTA or any of the EDTA complexes. Pseudomonas sp. mineralized calcium and iron citrates but had no activity on hydrogen, aluminum, or magnesium citrate. Pseudomonas pseudoalcaligenes mineralized calcium, iron, hydrogen, and aluminum citrates but had little activity on magnesium citrate. Pseudomonas alcaligenes used calcium, iron, hydrogen, and aluminum oxalates readily, but it used magnesium oxalate at a slower rate. Listeria sp. destroyed calcium NTA but had no effect on hydrogen, iron, or magnesium NTA. Increasing the Ca concentration in the medium enhanced the breakdown of NTA by Listeria sp. The different activities of the bacterial isolates were not a result of the toxicity of the complexes or the lack of availability of a nutrient element. NTA mineralization was not enhanced by the addition of Ca to Beebe Lake water, but it was enhanced when Ca and an NTA-degrading inoculum were added to water from an oligotrophic lake. The data show that chemical speciation influences the mineralization of organic compounds by naturally occurring microbial communities and by individual bacterial populations.

Journal Article↗
PubMed2002

The role of dietary microparticles and calcium in apoptosis and interleukin-1beta release of intestinal macrophages.

BACKGROUND & AIMS: The intestinal mucosa is exposed to micron-sized, man-made exogenous particles (e.g., titanium dioxide) and freshly formed endogenous particles (calcium phosphate). A role for such microparticles in inflammation has been proposed, and here we examined their effects on lamina propria mononuclear cells. METHODS: Lamina propria mononuclear cells were isolated from patients with and without inflammatory bowel disease and incubated with lipopolysaccharide, titanium dioxide, and calcium +/- citrate, as well as a conjugate of lipopolysaccharide, calcium, and titanium dioxide. Interleukin-1beta and interleukin-1 receptor antagonist were measured by enzyme-linked immunosorbent assay in culture supernatants and macrophage apoptosis by flow cytometry. Mechanistic studies were undertaken in normal peripheral blood mononuclear cells. RESULTS: Baseline levels of interleukin-1beta and macrophage apoptosis were greater in inflammatory bowel disease than in normal lamina propria mononuclear cells. Lipopolysaccharide and titanium dioxide had no additional effect, but calcium, and more so the conjugate, induced interleukin-1beta release in proportion to the degree of inflammation. Citrate, used to prevent in situ calcium phosphate formation, negated lamina propria mononuclear cell stimulation. Macrophage apoptosis was also increased by calcium and the conjugate. In peripheral blood mononuclear cells, inhibition of caspase 1 reduced interleukin-1beta secretion, whereas blockade of phagocytosis inhibited calcium-induced apoptosis and interleukin-1beta release. CONCLUSIONS: The endogenous luminal microparticle calcium phosphate Promotes apoptosis of intestinal macrophages. Concomitantly, interleukin-1beta is released, which is enhanced in the presence of inflamed cells and/or exogenous dietary microparticles. Endogenous or exogenous microparticles could aggravate the ongoing inflammation of inflammatory bowel disease.

Adolescent↗
PubMed1993

Pathophysiology of incomplete renal tubular acidosis in recurrent renal stone formers: evidence of disturbed calcium, bone and citrate metabolism.

Urinary acidification, bone metabolism and urinary excretion of calcium and citrate were evaluated in 10 recurrent stone formers with incomplete renal tubular acidosis (iRTA), 10 recurrent stone formers with normal urinary acidification (NUA) and 10 normal controls (NC). Patients with iRTA had lower plasma standard bicarbonate after fasting (P < 0.01) and lower urinary excretion of titratable acid (P < 0.05) and citrate (P < 0.01) compared with NUA patients and NC, and higher urinary excretion of ammonia (P < 0.05) compared with NC (P < 0.05). Hypercalciuria was found in 6 of 10 patients with iRTA compared with 3 of 10 with NUA, and 0 of 10 NC. The citrate/calcium ratio in urine was significantly reduced in iRTA compared with the value in NUA (P < 0.01), and in NUA compared with NC (P < 0.05). Biochemical markers of bone formation (serum osteocalcin) and bone resorption (urinary hydroxyproline) were significantly increased in iRTA compared with NUA and NC (P < 0.01), indicating increased bone turnover in stone formers with iRTA. Stone formers with iRTA thus presented with disturbed calcium, bone and citrate metabolism--the same metabolic abnormalities which characterize classic type 1 RTA. Mild non-carbonic acidosis during fasting may be a pathophysilogical factor of both nephrolithiasis and disturbed bone metabolism in stone formers with iRTA.

Acid-Base Equilibrium↗
PubMed2002

Relative bioavailability of calcium-rich dietary sources in the elderly.

BACKGROUND: The recent increase in the dietary calcium recommendation from 800 to 1200 mg/d for persons aged > 51 y has made it important to identify alternative high-calcium dietary sources that the elderly can use in meeting their calcium requirement. OBJECTIVE: We determined the bioavailability of calcium from 3 different sources: orange juice fortified with calcium-citrate malate, skim milk, and a calcium carbonate supplement. DESIGN: Twelve subjects [9 women and 3 men with a mean (+/- SEM) age of 70 +/- 3 and 76 +/- 6 y, respectively] consumed low-calcium (300 mg/d) and high-calcium (1300 mg/d) diets for three 1-wk periods each during a 6-wk crossover study. The acute biochemical response to calcium from each of the 3 sources was assessed during a 4-h period after the initial breakfast meal of the high-calcium diet. RESULTS: Postprandial suppression of serum parathyroid hormone did not differ significantly between the test meals containing calcium-fortified orange juice, the calcium carbonate supplement, and milk. This finding suggests that the calcium bioavailability from the 3 sources was equivalent. During the 1-wk high-calcium diet periods, fasting serum calcium increased by 3% (P < 0.0001), serum 1,25-dihydroxyvitamin D decreased by 20% (P < 0.0001), and a biomarker of bone resorption (serum N-telopeptide collagen cross-links) decreased by 14% (P < 0.02) compared with the low-calcium diet period. However, no differences among the supplemental calcium sources were found in these calcium-responsive measures or fasting serum parathyroid hormone concentration. CONCLUSIONS: In elderly subjects, the calcium bioavailability of the 3 high-calcium dietary sources tested was equivalent, during both the acute postprandial and longer-term periods.

Aged↗
PubMed2003

Effects of exercise on bone mineral density in calcium-replete postmenopausal women with and without hormone replacement therapy.

Osteoporosis is a major public health concern. The combination of exercise, hormone replacement therapy, and calcium supplementation may have added benefits for improving bone mineral density compared to a single intervention. To test this notion, 320 healthy, non-smoking postmenopausal women, who did or did not use hormone replacement therapy (HRT), were randomized within groups to exercise or no exercise and followed for 12 months. All women received 800 mg calcium citrate supplements daily. Women who exercised performed supervised aerobic, weight-bearing and weight-lifting exercise, three times per week in community-based exercise facilities. Regional bone mineral density (BMD) was assessed by dual energy X-ray absorptiometry. Women who used HRT, calcium, and exercised increased femoral neck, trochanteric and lumbar spine bone mineral density by approximately 1-2%. Trochanteric BMD was also significantly increased by approximately 1.0% in women who exercised and used calcium without HRT compared to a negligible change in women who used HRT and did not exercise. The results demonstrate that regional BMD can be improved with aerobic, weight-bearing activity combined with weight lifting at clinically relevant sites in postmenopausal women. The response was significant at more sites in women who used HRT, suggesting a greater benefit with hormone replacement and exercise compared to HRT alone.

Adult↗
PubMed1995

Anabolic effects of fluoride on bone.

Fluoride exerts a biphasic action at the level of osteoblasts, on bone mineral, on bone structure and function, and in the treatment of osteoporosis. At low circulating concentrations, skeletal uptake of fluoride is limited and the effects are beneficial. At higher concentrations and greater skeletal uptake, fluoride may cause the formation of abnormally mineralized bone of impaired quality. A new treatment program entailing intermittent slow release sodium fluoride (SR-NaF) with continuous calcium citrate may capture desirable qualities of fluoride without toxic effects, and be therapeutically efficacious in postmenopausal osteoporosis.

Antioxidants↗
PubMed1996

Lessening dental erosive potential by product modification.

Current interest in dental erosion has led to increasing attention to ways in which potentially erosive products might be modified. Information on how this could be achieved has been hard to gather, and has focused chiefly on possibilities in reformulating soft drinks. The bulk of the work published on this relates to calcium and phosphate supplementation, ranging from early experimentation on saturation of a demineralising medium with tricalcium phosphate, through tests of more soluble phosphates and other calcium salts providing various levels of Ca2+ and PO4(3-), to a calcium citrate malate additive specially formulated to curb erosion by soft drinks. Opinions on the effectiveness of citrate, the practicability of reducing the acidity levels of soft drinks, and the possible applications of fluoride, bicarbonates and certain constituents of milk products are also included. Finally, an attempt has been made to summarize some of the advantages and shortcomings of the different methods, but it is clear that much further work will be needed before firm guidelines on the best routes to product improvement can be laid down.

Acids↗
PubMed2006

Hyperoxaluria in women with vulvar vestibulitis syndrome.

OBJECTIVE: To determine whether evaluation and treatment of hyperoxaluria in vulvar vestibulitis syndrome (VVS) is justified. STUDY DESIGN: Forty women (mean age, 24.5 years; range, 18-35) diagnosed with VVS at a sex therapy clinic participated. Diagnosis of VVS relied upon Friedrich's criteria: (1) severe vulvar vestibular pain upon touch or attempted vaginal entry, (2) tenderness to pressure localized within the vulvar vestibule, and (3) physical findings confined to vulvar erythema of various degrees. Oxalate was measured in 24-hour urine samples. Women with hyperoxaluria (urine oxalate >50 mg/24 h) were placed on a low-oxalate diet and oral calcium citrate as single therapy and reevaluated 3 months later. RESULTS: Hyperoxaluria was diagnosed in 7 women (17.5%), of whom 1 demonstrated an objective improvement and could have pain-free vaginal intercourse following treatment, yielding a 2.5% benefit from the evaluation and treatment of hyperoxaluria. CONCLUSION: There is no justification for evaluation and treatment of hyperoxaluria in women with VVS due to its low yield and economic burden.

Adolescent↗
PubMed2005

Are we giving too much iron? Low-dose iron therapy is effective in octogenarians.

PURPOSE: Elderly patients are vulnerable to the dose-dependent adverse effects of iron replacement therapy. Our study examines whether low-dose iron therapy can efficiently resolve iron-deficiency anemia in patients over the age of 80 years and reduce adverse effects. SUBJECTS AND METHODS: Ninety hospitalized patients with iron-deficiency anemia were randomized to receive elemental iron in daily doses of 15 mg or 50 mg as liquid ferrous gluconate or 150 mg of ferrous calcium citrate tablets for 60 days. Thirty control patients without anemia were given 15 mg of iron for 60 days. A 2-hour iron absorption test was performed after the initial dose. Hemoglobin and ferritin levels were measured on day 1, 30, and 60 after initiating therapy. Each patient completed a weekly questionnaire regarding drug-induced adverse effects. RESULTS: Serum iron rose significantly in the anemic patients beginning 15 minutes after the first dose but not in nonanemic patients. Two months of iron treatment significantly increased hemoglobin and ferritin concentrations similarly in all 3 groups of iron-deficiency anemia patients (for example, hemoglobin levels rose from 10.0 g/dL to 11.3 g/dL with 15 mg/d of iron therapy and from 10.2 g/dL to 11.6 g/dL with 150 mg/d). Abdominal discomfort, nausea, vomiting, changes in bowel movements, and black stools were significantly more common at higher iron doses. CONCLUSIONS: Low-dose iron treatment is effective in elderly patients with iron-deficiency anemia. It can replace the commonly used higher doses and can significantly reduce adverse effects.

Aged↗
PubMedDate not supplied

Compatibility of common intravenous solutions with CPD blood.

Blood anticoagulated with CPD was mixed with lactated Ringer's solution, 5 per cent aqueous dextrose, 5 per cent dextrose in 0.225 per cent saline, 5 per cent dextrose in 0.9 per cent saline, and 0.9 per cent saline solution in varying concentrations and incubated at room temperature and 37 C. Clots formed in the blood-lactated Ringer's mixture after five minutes at a citrate:calcium molar ratio of 4:1 or lower. Aqueous dextrose-blood mixtures showed immediate clumping with gross hemolysis after 30 minutes incubation. Blood mixed with 5 per cent dextrose and 0.225 per cent saline hemolyzed within ten minutes incubation at 37 C. No hemolysis occurred in blood mixed with 5 per cent dextrose in 0.9 per cent saline or with 0.9 per cent saline. Traces of solutions labeled with Evans blue dye remained in intravenous administration tubing even 30 minutes after a simulated transfusion was begun. Lactated Ringer's solution and 5 per cent dextrose in 0.225 per cent saline should not be administered concurrently with blood. Lactated Ringer's solution may also be harmful when used to start transfusions as it rapidly produces clots when mixed with CPD blood.

Anticoagulants↗
PubMed2006

Calcium retention in adolescent boys on a range of controlled calcium intakes.

BACKGROUND: National calcium requirements in the United States for boys are based on data from girls. On average, boys develop larger skeletons than do girls, yet it is unknown whether the additional skeletal accretion in boys requires additional dietary calcium intake. OBJECTIVE: The objective was to determine calcium retention in adolescent boys in response to a range of controlled intakes and to compare the intake needed for maximal retention in boys with that needed in adolescent girls studied under the same conditions. DESIGN: Thirty-one boys aged 12-15 y participated in 3-wk metabolic balance studies testing a range (700-2100 mg/d) of calcium intakes in a crossover study design with a 2-wk washout period. Calcium intake was varied by using a beverage fortified with calcium citrate malate. After a 1-wk equilibration period, calcium retention was calculated as dietary calcium intake minus the calcium excreted in the feces and urine over the following 2 wk. The dietary intake at which maximal calcium retention occurred was determined by using a nonlinear regression model. The results in boys were compared with those obtained in 35 adolescent girls previously studied under the same protocol. RESULTS: Maximal calcium retention in boys was achieved at an intake of 1140 mg/d. Calcium retention was higher (by 171 +/- 38 mg/d) in boys than in girls at all calcium intakes studied. CONCLUSION: The higher calcium retention in boys than in girls was attained through higher net calcium absorption and lower urinary excretion than in girls.

Adolescent↗
PubMed1964

EFFECT OF HYDROCHLOROTHIAZIDE ON SERUM AND URINARY CALCIUM AND URINARY CITRATE.

Benzothiadiazines, potent oral diuretics, also inhibit carbonic anhydrase, although to a lesser degree than acetazolamide (Diamox). The latter has little effect on urinary calcium but causes hypocitriuria which predisposes to nephrolithiasis. The effect of benzothiadiazines on urinary calcium/citrate balance is less well known. In this study, the fall of urinary calcium and citrate was roughly 50% and 30%, respectively, in normal and hypertensive subjects during the prolonged administration of hydrochlorothiazide, a member of the benzothiadiazine family. Hence, in contradistinction to acetazolamide, this drug produces hypocalciuria but depresses the urinary citrate less. Consequently, the benzothiadiazines would not be expected to predispose to nephrolithiasis. In addition, hydrochlorothiazide was found to produce a 10-20% fall in creatinine clearance and an initial rise of roughly 0.7 mg./100 ml. in serum calcium concentration. There are indications that the benzothiadiazines affect the overall metabolism of calcium and citrate.

Acetazolamide↗
PubMed1991

Calcium acetate control of serum phosphorus in hemodialysis patients.

Calcium acetate has many characteristics of an ideal phosphorus binder. It is a readily soluble salt that avidly binds phosphorus in vitro at pH 5 and above. One-dose/one-meal balance studies show it to be more potent than calcium carbonate or calcium citrate. We studied chronic (3-month) phosphorus binding with calcium acetate in 91 hyperphosphatemic dialysis patients at four different centers. All phosphorus binders were stopped for 2 weeks. Calcium acetate at an initial dose of 8.11 mmol (325 mg Ca2+) per meal was then used as the only phosphorus binder. Dose was adjusted to attempt control of predialysis phosphorus level less than 1.78 mmol/L (5.5 mg/100 mL). Final calcium acetate dose was 14.6 mmol (586 mg) Ca2+ per meal. Sixteen patients developed mild transient hypercalcemia (mean, 2.84 mmol/L [11.4 mg/dL]. Initial phosphorus values in mmol/L (mg/dL) were 2.39 (7.4); at 1 month, 1.91 (5.9); and at 3 months, 1.68 (5.2). Initial calcium values in mmol/L (mg/dL) were 2.22 (8.9); at 1 month, 2.37 (9.5); and at 3 months, 2.42 (9.7). Initial aluminum values in mumol/L (micrograms/L) were 2.99 (80.7); and at 3 months were 2.54 (68.4). Initial C-terminal parathyroid hormone (C-PTH) values in ng/mL were 14.6; at 1 month, 11.9; and at 3 months, 13.2. Sixty-nine patients then entered a double-blind study. Phosphorus binders were stopped for 1 week. Calcium acetate (at a dose established in a prior study) or placebo was then administered for 2 weeks. Next, patients were crossed to the opposite regimen for 2 weeks. Initial phosphorus was 2.36 mmol/L (7.3 mg/100 mL) and calcium 2.22 mmol/L (8.9 mg/100 mL).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1997

Effect of dietary calcium on urinary oxalate excretion after oxalate loads.

An experimental model that allowed differentiation between endogenously and exogenously derived urinary oxalate was used to assess the effect of different forms and doses of ingested calcium on oxalate absorption and excretion. In replication 1 (R-1), subjects participated in three oxalate load (OL) tests: baseline (OL alone), calcium carbonate (OL with concomitant calcium carbonate ingestion), and calcium citrate malate (CCM) (OL with concomitant CCM ingestion). The calcium salts each provided 300 mg elemental Ca. OLs consisted of 180 mg unlabeled and 18 mg 1,2[13C2]oxalic acid. In R-2, subjects participated in four OL tests: baseline (OL alone) and OLs administered concomitantly with 100, 200, or 300 mg Ca. Timed urine samples after the OL were collected at 2-h intervals for the initial 6 h and samples were pooled into 9-h aliquots for the remaining 18 h of the 24-h period. In R-1, 24-h mean exogenous oxalate decreased (P < 0.05) after the OL from 36.2 mg (baseline) to 16.1 mg (after calcium carbonate) and to 14.3 mg (after CCM) whereas endogenous oxalate remained relatively constant. Mean 24-h oxalate absorption decreased significantly from that at the time of the baseline treatment (18.3%) after both calcium carbonate (8.1%) and CCM (7.2%) treatments. In R-2, mean 24-h oxalate absorption was significantly lower after 200 (5.9%) and 300 (7.6%) mg Ca than after 100 mg Ca (9.1%) and the OL alone (11.3%). Concomitant meal ingestion significantly decreased oxalate absorption in the absence of dietary calcium but not in association with the 300-mg Ca treatment. The overall data provide definitive evidence that dietary calcium can reduce oxalate absorption and excretion. Calcium carbonate and CCM were equally effective in this regard and a minimum of 200 mg elemental Ca maximized this effect in conjunction with an oxalic acid intake of 198 mg.

Absorption↗
PubMed1995

Urinary Tamm-Horsfall protein increased after potassium citrate therapy in calcium stone formers.

OBJECTIVES: To evaluate the effect of oral potassium citrate therapy on urinary excretion rates of citrate. Tamm-Horsfall protein (THP), and on calcium oxalate monohydrate crystal agglomeration inhibition [tm], in patients with recurrent calcium stone formation. METHODS: To evaluate the effect of oral therapy with potassium citrate on urinary citrate, THP, and [tm], 24-hour urine samples were collected before and at least 2 months after initiation of oral potassium citrate therapy in 33 calcium stone-forming patients who had no dietary restrictions. The citrate concentration was measured by an adaptation of a citrate lyase method. Urinary disaggregated THP concentration was determined with a quantitative enzyme-linked immunosorbent assay. The [tm] was determined by observing the effects of patients' urine, before and after oral potassium citrate therapy, on the uptake of 45Ca2+ onto the surfaces of added preformed calcium oxalate crystals in a supersaturated solution of calcium oxalate, using the in vitro kinetic method described by other investigators. RESULTS: We observed an increased urinary excretion rate of citrate from a mean of 1.9 mmol/24 h prealkali to 2.6 mmol/24 h postalkali (P < 0.0004) and of THP from a mean of 94.0 mg/24 h prealkali to 199.3 mg/24 h postalkali (P < 0.0016). A corresponding increase in [tm] from a mean of 177.1 minutes prealkali to 221.0 minutes postalkali (P < 0.024) was also observed. CONCLUSIONS: To our knowledge this is the first report correlating increased urinary citrate with THP excretion rate following oral alkalinization with potassium citrate in calcium stone formers. Of clinical importance is the corresponding increase in [tm], which was previously shown to be inversely related to stone-forming activity. Moreover, urinary citrate and THP are known to have a synergistic effect on [tm]. Our data suggest that the effectiveness of potassium citrate therapy in calcium stone-forming patients may, at least in part, be due to increased levels of THP.

Adult↗
PubMed1997

Calcium retention in relation to calcium intake and postmenarcheal age in adolescent females.

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.

Adolescent↗
PubMed1992

Hyperphosphatemia: its consequences and treatment in patients with chronic renal disease.

Control of phosphorus accumulation in chronic renal insufficiency is crucial to the prevention of secondary hyperparathyroidism and metastatic calcification. In early renal failure, calcitriol levels are normal and parathyroid hormone levels are elevated. The phosphorus levels are maintained in the normal range by the phosphaturia induced by hyperparathyroidism. In this situation, dietary phosphorus restriction increases calcitriol levels and suppresses parathyroid hormone secretion. As renal failure progresses into late stages, hyperphosphatemia is evident along with low levels of calcitriol and worsening hyperparathyroidism. Phosphorus restriction will not affect calcitriol concentrations, yet parathyroid levels may decline. During long-term dialysis, urinary excretion of phosphorus is usually minimal. Therefore, phosphorus balance is determined primarily by the net amount absorbed by the bowel and the quantity removed during dialytic therapy. Given an adequate diet, no form of conventional dialysis is able to fully compensate for the gastrointestinal absorption of phosphorus. Hence, compounds that bind phosphorus in the bowel are often necessary. With the realization that the use of phosphorus binders containing aluminum leads to aluminum accumulation and its sequelae: osteomalacia, dementia, myopathy, and anemia, other phosphorus binders have been evaluated. Calcium carbonate has been investigated the most thoroughly and is in wide use. It is inexpensive and contains a high percent of elemental calcium. However, it is only modestly potent in the binding of phosphorus, and large doses are often necessary to attain satisfactory control of phosphorus. This may lead to hypercalcemia. One approach to this problem is to decrease the concentration of calcium in the dialysate. Alternatively, a more effective phosphorus binder may be used. Calcium acetate has been shown in acute studies to have twice the binding capacity of phosphorus per calcium absorbed than calcium carbonate. Whether use of this compound decreases the incidence of hypercalcemia is unproven. Calcium citrate increases the gastrointestinal absorption of aluminum and offers no advantage over calcium carbonate. Other compounds, such as calcium ketoacids and calcium alginate, have not been extensively studied and are not generally available. The use of phosphorus binders containing magnesium in conjunction with a dialysate low in magnesium may be efficacious. Large doses of magnesium will cause diarrhea and thus limit its use as a single agent. Reasons for failure to control hyperphosphatemia include poor compliance, improper prescription of binders, poor dissolution rates seen with some generic brands of calcium carbonate, and the presence of severe hyperparathyroidism. Optimal control of serum phosphorus in dialysis patients should always be viewed in the context of adequate nutrition and protein intake.

Aluminum↗