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PubMed1983

Calcium and phosphorus metabolism during total parenteral nutrition.

Calcium and phosphorus metabolism and balance were studied in 151 patients receiving total parenteral nutrition (TPN). Hypercalciuria was common, with mean (+/- SD) urinary calcium excretion 17.5 +/- 3.9 meq/24 hours (n = 2610). There was a significant positive correlation between urinary calcium excretion and parenteral calcium intake (r = 0.34, p less than 0.001). There was also a positive correlation between calcium balance and parenteral calcium intake (r = 0.61, p less than 0.001) in patients without extra-renal losses. Positive calcium balance was achieved with parenteral calcium intake greater than 15 meq/24 hours. Urinary phosphorus excretion correlated positively with parenteral phosphorus intake (r = 0.50, p less than 0.001). Phosphorous balance also correlated positively with parenteral phosphorus intake (r = 0.78, p less than 0.001). Positive phosphorus balance was achieved with parenteral phosphorus intake above 15 mmol/24 hours. Fifty-three patients received 1,000 IU vitamin D once weekly and showed no significant change in serum calcium. Ninety-eight patients received 1,000 IU vitamin D twice weekly and showed a gradual but significant mean increase over time in serum calcium.

Adolescent↗
PubMed2003

The nephrologist's role in the management of calcium-phosphorus metabolism in patients with chronic kidney disease.

BACKGROUND: In patients with chronic kidney disease (CKD), timely referral to a nephrologist has been shown to improve outcomes, but the specific care measures mediating these superior outcomes have not been sufficiently described. METHODS: In a cohort of 3014 patients with CKD, we evaluated whether they had any indicators of calcium-phosphorus metabolism management prior to renal replacement therapy (RRT). These included measurement of parathyroid hormone (PTH) or vitamin D metabolites, or receipt of calcitriol or calcium-containing phosphate binders (CCPB) prior to RRT. Control patients without such care were selected by risk-set matching. We used multivariate conditional logistic regression analysis to test whether use of these interventions was associated with prior nephrologist consultation. We then used Cox proportional hazards models to assess whether implementation of such care was associated with differences in 1-year mortality once RRT was instituted. RESULTS: Only 3.4% of CKD patients had their PTH assessed prior to RRT, and 0.3% had vitamin D status measured. Use of calcitriol (12.2%) and CCPBs (16%) was slightly more prevalent. Seeing a nephrologist was highly associated with use of the tests and drugs studied (odds ratio, 1.28 to 6.46; all P values <0.001), but care by generalists or other specialists was not. Management of calcium-phosphorus metabolism was independently associated with a 35% decreased likelihood of death (hazards ratio=0.65; 95%CI, 0.51 to 0.84) in the first year of RRT. CONCLUSION: Improvements in management of calcium-phosphorus metabolism in patients with CKD are attributable to nephrologist care and appear to mediate the survival benefit seen in patients who see a nephrologist relatively early in the course of their CKD.

Aged↗
PubMed1982

Effect of small doses of aluminum-containing antacids on calcium and phosphorus metabolism.

The effect of small doses of four commercially available aluminum-containing antacids on calcium and phosphorus metabolism was investigated in adult males in 20 studies. During the use of these doses of antacids, urinary and fecal calcium increased significantly during a low calcium intake averaging 252 mg/day, and the calcium balances became distinctly more negative. There was a reversal of the normal pattern of phosphorus excretions, namely, the fecal phosphorus was high and the urinary phosphorus was low. During a normal calcium intake of 800 mg/day, these doses of antacids did not result in significant changes of the calcium excretions or balance. Despite the decrease in net intestinal absorption of calcium, the average 47Ca absorption remained unchanged, irrespective of the type and dose of antacid used. In three patients who received large therapeutic doses of antacids, 240 to 450 ml/day, the changes of calcium and phosphorus metabolism were intensified.

Adult↗
PubMed2001

Treatment of calcinosis in juvenile dermatomyositis with probenecid: the role of phosphorus metabolism in the development of calcifications.

OBJECTIVE: To report the efficacy of probenecid for calcinosis of juvenile dermatomyositis (JDM) and assess the changes in phosphorus metabolism during treatment. METHODS: Biochemical studies of calcium and phosphorus metabolism were performed in a 9-year-old girl with JDM and extensive calcifications before and during probenecid treatment. RESULTS: The calcifications resolved over 18 months of treatment. Probenecid was found to be effective in reducing calcifications by increasing renal phosphate clearance. CONCLUSIONS: The tendency for calcifications in some patients with JDM might be related to an increase in renal phosphate reclamation, and therefore, probenecid treatment may be effective in these patients.

Calcinosis↗
PubMed1985

[Comparative effects of magnesium deficiency and overload on calcium and phosphorus metabolism in the growing pig].

This study was designed to assess the influence of dietary magnesium on calcium and phosphorus metabolism in growing pigs. 18 4-month-old pigs received either an Mg-deficient (40 ppm), an Mg overload (5,600 ppm) or a control Mg diet (1,000 ppm) for 70 days. The following parameters were measured: kinetics of plasma concentrations of Ca, phosphates, Mg and alkaline phosphatase (AP), absorptions, urinary and fecal excretions, retentions of Ca, P and Mg, soft tissue and bone mineral contents (BMC), and intestinal mucosal CaBP (calcium-binding protein) and AP activities. Dietary Mg level had no effect on calcium and phosphorus metabolism as far as Ca and P absorptions and retentions, BMC, intestinal CaBP and plasma levels of Ca, P and AP are concerned. Mg overload significantly decreased urinary P excretion and increased kidney P content, but did not change fecal P excretion. Jejunal AP activity was slightly decreased in Mg-deficient pigs. The plasma, bone, urinary, fecal, absorbed and retained Mg varied linearly with Mg intake (r: 0,85-0.96). In Mg-deficient pigs, hypomagnesemia appeared after 1 week and its severity did not increase with time. In Mg-overloaded pigs, hypermagnesemia occurred very late and was limited. This suggests that, in the growing pig, dietary Mg has little or no effect on Ca-P metabolism. It may also be concluded that growing pigs are rather resistant to Mg deficiency since no clinical symptoms were observed.

Alkaline Phosphatase↗
PubMed1994

Effects of perfluoro-n-octanoic acid, perfluoro-n-decanoic acid, and clofibrate on hepatic phosphorus metabolism in rats and guinea pigs in vivo.

Phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy was used to study the effects of perfluoro-n-octanoic acid (PFOA), perfluoro-n-decanoic acid (PFDA), and clofibrate (CLOF) on liver phosphorus metabolism in rats and guinea pigs in vivo. All three compounds are known to cause peroxisome proliferation in rats but not in guinea pigs. The data indicate that indices related to overall tissue viability (i.e., adenosine triphosphate levels) remain unaffected at the doses and experimental times investigated for all treatments and both species. PFDA-treated rats revealed a marked increase in a liver phosphomonoester resonance compared with corresponding controls (p < or = 0.01); no such effect was observed in guinea pigs. This particular 31P NMR signal was identified as phosphocholine (PCho) and was found to steadily increase in concentration at consecutive days post-PFDA treatment, reaching 6.26 +/- 0.29 mumol/g liver at 5 days. This is fourfold greater than the PCho levels determined in livers from corresponding pair-fed control rats. The elevation in liver PCho is a specific response of PFDA treatment in rats and is not simply related to peroxisome proliferation in general, since neither PFOA nor CLOF produce such an effect. The data suggest a unique effect of PFDA on liver phospholipid metabolism, specifically phosphatidylcholine, which may involve enhanced phospholipid turnover via phosphatidylcholine-specific phospholipase C activity.

Animals↗
PubMed1984

Responses in calcium and phosphorus metabolism and hepatic lipid deposition among estrogenized chicks fed various dietary ingredients.

The purpose of this study was to determine whether diet composition would influence calcium and phosphorus metabolism in chicks administered estrogen. At 1 day of age, broiler chicks were fed either a corn-soybean meal diet (CS), or an isoenergetic and isonitrogenous diet containing 5% fish meal, 5% alfalfa meal and 10% torula yeast (FAY). At 21 days equivalent numbers were implanted with one of two lengths of Silastic tubing containing estradiol dipropionate, while the remaining birds served as nonimplanted controls. Significant increases were observed in liver weight, liver lipid, plasma total calcium and inorganic phosphate in chicks that were implanted, while concomitant declines were seen in body weight. Implanted chicks fed the CS diet had significantly higher liver weight, liver lipid, plasma phosphorus and plasma calcium and lower tibial bone ash than those fed the FAY diet. Furthermore, liver lipid values were very highly correlated with plasma phosphorus and calcium. In an identical study with slower growing White Leghorn chicks, the same trends were observed but were less well defined. These data show that the inclusion of certain ingredients into corn-soybean diets balanced for the major nutrients affects the response of chicks to estrogenization. Liver lipid deposition, calcium and phosphorus metabolism are all subject to diet and estrogen interactions.

Animals↗
PubMedDate not supplied

Calcium and phosphorus metabolic changes in children with hepatic bilharziasis.

Investigations were done to study the calcium and phosphorus metabolic changes in 35 children with hepatic bilharziasis, of whom 12 were ascitic. Thirteen normal children served as controls. Despite a normal serum level of both calcium and inorganic phosphate in the Bilharzial group, yet both were increased in urine. The mean values obtained from the ascitic fluid were 70% and 90.2% of their serum levels, respectively. The corrected creatinine clearance was significantly diminished, while PEI was significantly increased, and the % TRP significantly decreased, with still a more marked decrease in the ascitic cases. Following a phosphate lead the serum inorganic phosphate level showed a significantly more rapid lowering in both bilharzial groups, as compared to the control group. On the other hand bilharzial cases responded to the intravenous calcium load by a significant retention of calcium in the serum.

Adolescent↗
PubMed1990

[Are there abnormalities of parathormone, calcium and phosphorus metabolism in hypertrophic cardiomyopathy?].

The importance of calcium and phosphorus metabolism for the development of hypertrophic cardiomyopathies is still obscure. Therefore 52 patients with hypertrophic cardiomyopathy were subjected to detailed cardiological and laboratory examinations. Twenty-five age matched healthy subjects served as controls. The following indicators were assessed: calcium and its ionized fraction, phosphorus, chlorides and magnesium in serum and 24 h urine, as well as AST, ALT, ALP, ACP, urea, creatinine, protein electrophoresis (to check calcium values with regard to serum albumins), endogenous creatinine clearance, Palmer's chloride phosphate index and Nordin's index. In addition to tubular phosphate reabsorption, the renal phosphate threshold was assessed and finally the parathormone blood level by the RIA method. In patients with hypertrophic cardiomyopathy a significant increase of the parathormone level was found--in a total of seven patients with advanced myocardial hypertrophy (more than 30 mm). There were no significant differences in the remaining parameters. It may thus be admitted that in some instances the increased parathormone level may cause an increase of the already existing myocardial hypertrophy. However, in the broad spectrum of patients with hypertrophic cardiomyopathy it is not suited for explaining morphological findings.

Adolescent↗
PubMed1986

Calcium and phosphorus metabolism in chronically vitamin D-deficient laboratory rabbits.

Calcium and phosphorus metabolism were investigated in chronically vitamin D-deficient adult albino rabbits that were consuming a diet containing 1% calcium and 0.5% phosphorus. Mineral balances, net intestinal and renal handling of calcium and phosphorus, and serum concentrations of calcium, phosphorus, parathyroid hormone, 25-hydroxycholecalciferol, and calcitriol were measured during metabolic balance studies. Chronic vitamin D deficiency (with undetectable serum concentrations of 25-hydroxycholecalciferol or calcitriol) was associated with mild hypocalcemia, moderate hypophosphatemia, and generally elevated serum parathyroid hormone concentrations. Net intestinal absorption of calcium or phosphorus was equal in chronically vitamin D-deficient adult rabbits and nutritionally matched, vitamin D-supplemented controls. In contrast, urinary excretion rates of both minerals were reduced significantly in the vitamin D-deficient group, indicating the action of homeostatic mechanisms within the kidneys. As a result of the decreased urinary excretions of calcium and phosphorus, the net external balance for each mineral during the metabolic balance studies was significantly more positive in the chronically vitamin D-deficient rabbits than in the vitamin D-supplemented controls. These observations demonstrate the importance of the renal conservation of Ca and P to mineral homeostasis in the chronically vitamin D-deficient adult rabbit.

Animals↗
PubMed2004

The role of abnormal phosphorus metabolism in the progression of chronic kidney disease and metastatic calcification.

The role of abnormal phosphorus metabolism in the progression of renal disease and metastatic calcification. Hyperphosphatemia is a common biochemical abnormality in advanced renal failure. The resulting increase serum calcium x phosphorus product results in the deposition of hydroxyapatite crystals. The crystalline properties of these deposits incite an inflammatory response manifested by encapsulated tumoral deposits around joints, acute inflammatory arthritis, and irritative conjunctivitis. These deposits occur in association with marked elevation of serum phosphorus levels, and are prevented and eradicated by normalizing serum phosphorus levels. The calcium-phosphate deposits which occur in heart and lungs are nonapatitic. These deposits were never clearly related to hyperphosphatemia. They are mainly of historic interest because currently they are rarely seen. Their eradication appears to be more of a result of improved dialytic techniques than correction of serum phosphorus levels. The presence, persistence, and progression of vascular calcification are more closely related to patient age and duration of dialysis than hyperphosphatemia. This suggests that these deposits are a result of dystrophic calcification occurring de novo in a diseased or damaged vessel wall. Phosphorous restriction has also been shown to be protective of renal functional deterioration in experimental renal disease. It is unclear whether the protective effect is mediated through phosphate restriction or phosphate depletion. In conclusion, control of serum phosphorus levels in dialyzed uremic patients has clearly decreased morbidity associated with periarticular, articular, and conjunctiva hydroxyapatite deposits. In contrast, phosphorous control has had little effect on the presence or severity of vascular calcification.

Calcinosis↗
PubMed2003

Intracellular phosphorus metabolism of Microcystis aeruginosa under various redox potential in darkness.

Phosphorus metabolism of Microcystis aeruginosa was studied under gradient redox potential from 252 mV to -70 mV in darkness. The release of phosphorus occurred in all the treatments, and this process was accelerated in darkness when the redox potential was lowered. Low redox potential in darkness stimulated the accumulation of polyphosphate (PolyP) and the degradation of polyglucose. The synthesis of PolyP delayed the decrease of intracellular orthophosphate. The death of M. aeruginosa was slowered when the redox potential was low in darkness. The accumulation of PolyP under low redox potential in the dark was very important to M. aeruginosa for endurance through the unfavorable growth conditions for maintaining phosphorus concentration, energy storage, and other physiological functions. The ability to accumulate PolyP in the dark and negative redox potential may be of considerable advantage in the low-light, organically rich, and low-redox habitats.

Anaerobiosis↗
PubMed1986

Studies on the mechanism of diet-induced nephrocalcinosis: calcium and phosphorus metabolism in the female rat.

The disposition of calcium and phosphorus in female Sprague-Dawley rats fed either a low- or a high-calcium semi-synthetic diet for up to 9 wk from weaning has been investigated. The rats fed the low-calcium diet (calcium to phosphorus ratio approximately 1:1) developed cortico-medullary nephrocalcinosis within 6 wk, whereas those fed the high-calcium diet (calcium to phosphorus ratio greater than 1.5:1) did not develop any lesion during this time. Intake and excretion of calcium was greater at all times in the animals fed the high-calcium diet than in those on the low-calcium diet. However, the true absorption and retention of calcium was not significantly different between the two diet groups. Phosphorus intake and total excretion were similar for both groups of animals, although urinary excretion accounted for less than 1% of the total in the animals fed the high-calcium diet but more than 50% in those fed the low-calcium diet. Bioavailability of phosphorus decreased with age in both groups. Recovery of injected 45Ca in urine and faeces increased during the experimental period from approximately 3 to 11% of the dose in rats on the low-calcium diet and from approximately 9 to 13% in the high-calcium group. Recovery of both injected and orally administered 32P was substantially greater in the low-calcium group than in the high-calcium group at wk 3 and 5, but at wk 9 was only greater after intramuscular administration. At the earlier times the urine was the major route of 32P excretion. It appears that no gross disturbances of calcium or phosphorus metabolism occurred in female rats maintained on a diet that resulted in the rapid development of kidney calcification.

Absorption↗
PubMed1992

Magnetic resonance spectroscopy studies on experimental murine and human tumors: comparison of changes in phosphorus metabolism with induced changes in vascular volume.

The responses of two experimental murine tumors and two human tumor xenografts to the vasodilator hydralazine were compared using two magnetic resonance spectroscopy endpoints. Changes in tumor metabolism were determined using 31P MRS where inorganic phosphate levels relative to total phosphate (Pi/total) were measured, and alteration in tumor blood volume was examined using 19F MRS with perfluorooctylbromide (PFOB) as tracer. The integrated 19F signal from PFOB is dose dependent and stable for at least 2 hr after injection. The murine tumors SCCVII/Ha and KHT both showed changes in tumor metabolism after hydralazine, as an increase in Pi/total. However, hydralazine reduced vascular volume in the KHT tumor, demonstrated by reduced 19F signal from PFOB, but no such reduction was seen in the SCCVII/Ha tumor. In contrast, hydralazine had no effect on phosphorus metabolism in the HT29 and HX118 human tumor xenografts, but reduced vascular volume in both tumors. These results demonstrate that the effects of vasoactive agents such as hydralazine on tumor phosphorus metabolism are only partially consistent with changes in vascular volume, measured by the 19F MRS technique.

Animals↗
PubMed1975

[Isoprenaline, propranolol and in vivo phosphorus metabolism of the rat salivary gland].

Chronic treatment with isoprenaline causes hypersecretion and a marked enlargement of submaxillary glands. Isoprenaline, given to normal rats or treated animals with hypertrophied salivary glands, increases the incorporation of 32P in tissue inorganic and organic phosphates and phospholipids. Propranolol given alone is inactive on phosphorus metabolism, but inhibits the effect of isoprenaline. The phospholipid effect is probably related to the increase of membranes in hypertrophied acinar cells; a correlation with the hypersecretion induced by isoprenaline needs further study. The results show that in experimental sialadenosis and hypersialorrhea induced by isoprenaline in the whole rat stimulation of glandular beta-adrenoreceptors and phosphorus metabolism are involved.

Animals↗