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PubMed1987

Sequential calcium and phosphorus balance studies in preterm infants.

Forty-six infant boys less than 1500 g at birth and less than 32 weeks gestation were fed enterally from birth until day 47. Cohorts were given milk formula varying in calcium and phosphorus content: group A, calcium 45 mg/dL, phosphorus 33 mg/dL; group B, calcium 85 mg/dL, phosphorus 33 mg/dL; group C, calcium 125 mg/dL, phosphorus 33 mg/dL; group D, calcium 125 mg/dL, phosphorus 50 mg/dL; and group E, calcium 125 mg/dL, phosphorus 64 mg/dL. Three-day balance studies were begun at days 10, 20, 30, and 40. Calcium net absorption and retention were influenced by postnatal age and calcium intake. Calcium retention best approached intrauterine accretion rates in group C. Phosphorus was well absorbed irrespective of the calcium content of the milk. Phosphorus retention increased with increments in the calcium content of the milk. Increasing the phosphorus content of the milk (groups D and E) resulted in no overall change in calcium absorption and retention but some increments in phosphorus retention.

Birth Weight↗
PubMed1996

Use of sheep maintained by intragastric infusion as a model for studying the endogenous loss of phosphorus in ruminants.

Mature sheep fitted with a rumen cannula and an abomasal catheter were used to evaluate whether sheep maintained by intragastric infusion could be used as a model for studying minimum endogenous phosporus loss in ruminants. In control periods the sheep received 1.29 g phosphorus day-1 by infusion and maintained phosphorus balance. The withdrawal of phosphorus from the infusate led to a reduction in the excretion of phosphorus to 6.4 mg kg liveweight-1 day-1, a level lower than that currently used to estimate maintenance phosphorus requirements. However, salivary phosphorus secretion, based on rumen phosphorus outflow, averaged only about 1.2 g day-1, a level which would be considered insufficient to meet rumen microbial requirements in a normally fed animal. Allowing the sheep access to a small amount of roughage, although contributing little additional phosphorus, greatly increased salivary phosphorus flow and increased their endogenous excretion of phosphorus to levels close to those used to estimate maintenance requirements. These results suggest that this technique may offer an alternative way of measuring minimum endogenous mineral loss to those currently in use.

Abomasum↗
PubMed2003

Modeling of phosphorus dynamics in aquatic sediments: II--examination of model performance.

A sediment phosphorus model, describing dynamics of organic phosphorus, dissolved reactive phosphorus and exchangeable particulate phosphorus, is applied to five monitoring stations in Chesapeake Bay, USA, to examine model performance in predicting sediment-water phosphorus exchange. The model was fit to 1 year of field measurements, and verified over 3 years at five sampling stations. The results show that the simulated concentrations of phosphorus reasonably correspond to model mechanisms and field observations in both spatial and temporal variations. Predicted release fluxes of phosphorus are consistent with field measurements and improved over those obtained by existing sediment phosphorus models. The model incorporates the effects of dissolved oxygen and non-linear, non-equilibrium sediment sorption in phosphorus dynamics. A sensitivity analysis indicates the importance of the non-linear, non-equilibrium sorption processes to accurate prediction of sediment-water phosphorus flux.

Environmental Monitoring↗
PubMed2006

Organic phosphorus sequestration in subtropical treatment wetlands.

Diffuse phosphorus pollution is commonly remediated by diverting runoff through treatment wetlands to sequester phosphorus into soil layers. Much of the sequestered phosphorus occurs in organic forms, yet our understanding of its chemical nature is limited. We used NaOH-EDTA extraction and solution 31P NMR spectroscopy to speciate organic phosphorus sequestered in a large treatment wetland (STA-1W) in Florida, USA. The wetland was constructed on previously farmed peat and was designed to remove phosphorus from agricultural runoff prior to discharge into the Everglades. Unconsolidated benthic floc that had accumulated during the 9-year operation of the wetland was sampled along transects through two connected cells dominated by cattail (Typha dominigensis Pers.) and an additional cell colonized by submerged aquatic vegetation, including southern water nymph (Najas guadalupensis(Spreng.) Magnus) and coontail (Ceratophyllum demersum L.). Organic phosphorus was a greater proportion of the sequestered phosphorus in the cattail marsh compared to the submerged aquatic vegetation wetland, but occurred almost exclusively as phosphate diesters and their alkaline hydrolysis products. Itwas therefore markedly different from the organic phosphorus in mineral soils, which is dominated typically by inositol phosphates. Phosphate diesters are readily degradable in most soils, raising concern about the long-term fate of organic phosphorus in treatment wetlands. Further studies are now necessaryto assess the stability of the sequestered organic phosphorus in response to biogeochemical and hydrological perturbation.

Ecosystem↗
PubMed1984

Phosphorus administration in patients with profound hypophosphatemia.

The influence of severe hypophosphatemia (less than or equal to 1.0 mg/dl) on vitamin D metabolism was prospectively determined in 11 patients before and after intravenous phosphorus administration. Evidence of liver dysfunction was present in ten patients. The mean (+/- SE) plasma 25 hydroxycholecalciferol [25(OH)D] was significantly decreased before phosphorus therapy when compared to control subjects (9.4 +/- 1.3 vs. 17.8 +/- 1.3 ng/ml, P less than 0.001). With phosphorus administration, serum phosphorus increased from 0.59 +/- 0.07 to 2.58 +/- 0.09 mg/dl while 1,25 dihydroxycholecalciferol [1,25(OH)2D] decreased from 34.6 +/- 4.3 to 14.3 +/- 2.9 pg/ml (P less than 0.001). Plasma 25(OH)D, plasma immunoreactive PTH (both amino and carboxyterminal) and serum calcium did not change after phosphorus administration, suggesting that phosphorus alone was responsible for the change in plasma 1,25(OH)2D concentration. An inverse correlation was found between serum phosphorus and plasma 1,25(OH)2D (r = -0.62, P less than 0.005). In addition, a direct correlation was observed between plasma 25(OH)D and 1,25(OH)2D both before (r = 0.66, P less than 0.005) and after (r = 0.74, P less than 0.005) phosphorus administration. Thus, the decrease in 1,25(OH)2D levels with phosphorus therapy suggests a role of serum phosphate in the regulation of this sterol, and hypophosphatemia or phosphorus depletion may change the relationship of substrate [25(OH)D] to product [1,25(OH)2D].

Adult↗
PubMed1986

The absorption of dietary phosphorus and calcium in hemodialysis patients.

Absorption of dietary phosphorus plays a critical role in the development of metabolic bone diseases in patients with chronic renal failure. However, phosphorus absorption is difficult to quantitate in dialysis patients because the dialysis treatments complicate metabolic balance studies. Utilizing a recently developed technique which permits measurement of net absorption of dietary constituents after a single meal, we measured phosphorus absorption in dialysis patients. The following observations were made: A.) Following a meal containing approximately 300 mg phosphorus, mean phosphorus absorption in five hemodialysis patients (with severe vitamin D deficiency) was only slightly less than in matched controls (186 +/- 35 vs. 242 +/- 30). B.) After dialysis patients were treated with 1,25(OH)2-D3, phosphorus absorption increased from 186 +/- 35 to 272 +/- 16 mg (P less than 0.025). C.) The effect of three aluminum containing antacids on phosphorus absorption was studied; each slightly reduced the absorption of phosphorus compared to placebo (P less than 0.01), but there was no significant difference between them. D.) Aluminum hydroxide and calcium carbonate each reduced dietary phosphorus absorption to approximately the same extent. Calcium carbonate ingestion was associated with sharply increased calcium absorption. The absorption of dietary phosphorus is influenced only modestly by 1,25(OH)2-D3 and is inhibited to an equal but only modest degree by various aluminum antacids and by calcium carbonate.

Adult↗
PubMed1974

Role of 1,25-dihydroxyvitamin D3 in maintaining serum phosphorus and curing rickets.

The intravenous injection of a single dose of 650 pmoles of 1,25-dihydroxyvitamin D(3) to rats fed a vitamin D-deficient, low-phosphorus diet caused an elevation of serum phosphorus within 5 hours which reached a maximum in about 10-12 hours. This elevated serum phosphorus returned to deficiency levels 2-3 days later. On the other hand, a single injection of 650 pmoles of 25-hydroxyvitamin D(3) produced a significant rise at 12 hours, reached a maximum in 24-36 hours, and was maintained for at least 7 days. The single dose of 1,25-dihydroxyvitamin D(3) supported little calcification of bone, whereas the 25-hydroxyvitamin D(3) produced marked calcification. Six-hundred and fifty pmoles of 24,25-dihydroxyvitamin D(3) increased serum phosphorus only slightly and induced no calcification. When 1,25-dihydroxyvitamin D(3) was given each day, a sustained increase in serum phosphorus and marked bone calcification resulted. In contrast to the serum phosphorus responses, intestinal calcium transport remained high 5 days after administration of a single dose of 1,25-dihydroxyvitamin D(3). Serum calcium was not changed appreciably by any of the metabolites. Thyroparathyroidectomized rats or rats fed a diet extremely deficient in phosphate still exhibited a marked elevation of serum phosphorus in response to 1,25-dihydroxyvitamin D(3). The effect of 1,25-dihydroxyvitamin D(3) on serum phosphorus was greatly reduced in nephrectomized rats, suggesting that the serum phosphorus response to 1,25-dihydroxyvitamin D(3) may arise from an enhancement of phosphate reabsorption in the renal tubules. It is suggested that 1,25-dihydroxyvitamin D(3) cures rickets in rats by increasing the concentration of serum phosphorus rather than by increasing serum calcium concentration and calcium absorption.

Animals↗
PubMed2006

Chemical removal and recovery of phosphorus from excess sludge in a sewage treatment plant.

We describe a process for the recovery of phosphorus from excess sludge in a sewage treatment plant that currently uses polyaluminium chloride for chemical phosphorus removal. Instead, we employed alkaline dissolution of excess sludge with calcium phosphate precipitation to recover phosphorus from sewage. The recovery ratio for phosphorus from sewage using the phosphorus recovery system is approximately 50%. In addition, the amount of excess sludge in the phosphorus recovery system is approximately half that of conventional chemical phosphorus removal. Alkaline dissolution of excess sludge resulted in dissolution of aluminium into the supernatant. Furthermore, since dissolved aluminium can be reused as a coagulant, the phosphorus recovery system could be used to economize coagulant consumption. Operation and maintenance costs of the phosphorus recovery system are 25.9 U.S. cents per 1 m3 of sewage compared to 32.0 U.S. cents per 1 m3 of sewage for conventional chemical phosphorus removal, representing a decrease of 20% in the operation and maintenance costs.

Aluminum Chloride↗
PubMed1996

Changing phosphorus content of the U.S. diet: potential for adverse effects on bone.

The dietary intake of phosphorus in the United States is high relative to calcium. Intake estimates from the 1989-1991 Continuing Surveys of Food Intakes by Individuals conducted by the U.S. Department of Agriculture show that for both men and women, median calcium intakes do not meet the 1989 Recommended Dietary Allowances (RDAs) for most age groups over 10 y of age, whereas phosphorus intakes exceed the RDAs for most age groups. The use of phosphorus-containing food additives in the processing of foods contributes substantially to the daily phosphorus intake, and their use is increasing. Because much of the phosphorus through food additive use is not reflected in the estimates of phosphorus intakes derived from national food consumption surveys, these estimates underestimate true dietary intakes of phosphorus. High phosphorus intake has been shown to cause secondary hyperparathyroidism and bone loss in several animal models. High phosphorus, low calcium consumption consistent with current observed intake levels resulted in changes in calcium-regulating hormones that were not conducive to optimizing peak bone mass in young women. Evidence that such high phosphorus intakes may impair synthesis of the active metabolite of vitamin D and disrupt calcium homeostasis particularly in older women are discussed.

Animals↗
PubMed1998

Effects of oral phosphorus supplementation on mineral metabolism of renal transplant recipients.

BACKGROUND: Persistent hyperparathyroidism (HPT) is frequently observed in kidney transplant recipients. Hypophosphataemia is a common biochemical consequence of HPT. Theoretically, oral phosphorus administration may induce negative effects on the control of HPT, though this point has never been demonstrated in kidney-transplant recipients. This study was designed to evaluate the effects of oral phosphorus supplementation on the mineral metabolism of successful kidney transplant recipients. METHODS: Thirty-two kidney transplant recipients with serum creatinine < 2 mg/dl and serum phosphate levels <3.5 mg/dl were included in the study. After a washout period in which oral phosphorus supplementation was discontinued, the following parameters were determined (F0 period): serum calcium, phosphate, alkaline phosphatase, uric acid, bicarbonate, PTH, 1,25-dihydroxyvitamin D3 (1,25 (OH)(2)D) and 25-hydroxyvitamin D3 (25OHD). Creatinine clearance, calcium, and phosphate excretion were determined from a 24-h urine sample. The same determinations were repeated (F1 period) after all patients received 1.5 g of oral phosphorus for 15 days. For data analysis, patients were divided into two subgroups (optimal and suboptimal) according to allograft function (Ccr>or < 70 ml/min/1.73 m2). RESULTS: In the F0 period, only nine of 32 patients had PTH levels within the normal range (<65 pg/ml). The mean concentrations of PTH, 1,25(OH)(2)D and 25OHD were 132+/-97pg/ml, 40.5+16pg/ml and 12.5+/-8.2 ng/ml respectively. Phosphorus supplementation led to significant reductions in serum calcium and 1,25(OH)(2)D concentrations, as well as in urinary calcium excretion in the whole group. On the contrary, serum phosphate, PTH, and urinary phosphate excretion increased significantly. The percentage increase in PTH concentrations after phosphorus supplementation were similar in patients with optimal and suboptimal allograft function (33 vs 36%). The reduction of 1,25 (OH)(2)D concentrations after phosphorus supplementation was observed mainly in the subgroup with optimal allograft function (21% reduction with respect to baseline values), while the mean 1,25(OH)(2)D concentrations in patients with suboptimal allograft function scarcely changed (1.4% increase). Changes in 1,25(OH)(2)D concentrations after phosphorus supplementation, expressed as a percentage of the initial concentrations, correlated positively with the percentage changes in PTH concentrations for the whole group, as well as for each subgroup. The best determinants for the percentage and the absolute increase in PTH concentration after phosphorus supplementation was the final serum phosphate concentration (F=4.84, r=0.37, P=0.035) and the increase in serum phosphate (F=7.69, r=0.45, P= 0.009) respectively. CONCLUSIONS: Oral phosphorus supplementation led to a significant increase in the PTH concentration of kidney transplant recipients. The mean 1,25(OH)(2)D concentration decreased mainly in recipients with optimal allograft function. The counterbalance effect of PTH on 1,25(OH)(2)D production may account for the relative preservation of 1,25(OH)2D levels in recipients with suboptimal allograft function.

Administration, Oral↗
PubMed1998

Effect of RenaGel, a non-absorbed, calcium- and aluminium-free phosphate binder, on serum phosphorus, calcium, and intact parathyroid hormone in end-stage renal disease patients.

BACKGROUND: Control of dietary phosphate absorption in end-stage renal disease patients is essential to prevent the deleterious sequelae of phosphorus retention. Efficacy of currently available calcium- and aluminium-containing phosphate binders is constrained by the side-effects associated with the absorption of calcium and aluminium. The current study examined the efficacy of RenaGel, a calcium- and aluminium-free, polymeric phosphate binder, in end-stage renal disease patients. METHODS: Administration of calcium- or aluminium-containing phosphate binders ceased during a 2-week washout period. RenaGel, at starting doses of one, two, or three 500-mg capsules three times per day with meals, was administered for 8 weeks. RenaGel dose was titrated up 1 capsule per meal at the end of each 2-week period if necessary to achieve phosphorus control. A second 2-week washout period followed the end of RenaGel treatment. RESULTS: Mean serum phosphorus rose from a pre-washout level of 6.9 mg/dl (2.23 mmol/l) to 8.1 mg/dl (2.62 mmol/l) at the end of the initial 2-week washout. With RenaGel treatment, serum phosphorus declined and returned to pre-washout levels after 4 weeks. Serum phosphorus reached a nadir of 6.5 mg/dl (2.10 mmol/l) after 7 weeks of RenaGel treatment. Serum phosphorus rose to 8.2 mg/dl (2.65 mmol/l) 2 weeks after cessation of RenaGel treatment. As anticipated, calcium declined during the initial washout period when calcium-based phosphate binders were stopped for the majority of patients. The rise in serum phosphorus and decline in serum calcium during washout resulted in an increase in median intact parathyroid hormone (iPTH) levels from 292 pg/ml to 395 pg/ml. iPTH fell to 283 pg/ml after 6 weeks of RenaGel treatment despite a persistently lower serum calcium. RenaGel treatment also reduced serum total and LDL cholesterol by 25 mg/dl (0.65 mmol/l) and 23 mg/dl (0.59 mmol/l) respectively. CONCLUSIONS: RenaGel appears to be an effective phosphate binder free of calcium and aluminium. Phosphorus control with two to four RenaGel capsules per meal appears to result in comparable phosphorus lowering seen with calcium- or aluminium-based phosphate binders. RenaGel may offer an alternative for the control of phosphorus retention in end-stage renal disease patients.

Adult↗
PubMedDate not supplied

Effects of different phosphorus sources in the diet on bone composition and stability (breaking strength) in broilers.

In two fattening trials (in each 100 broilers kept in four groups with 25 animals) as well as in a balance trial (four groups with four broilers in a group) the effects of inorganic phosphorus sources [monocalcium phosphate (MCP), dicalcium phosphate (dihydrate; DCP) and defluorinated phosphate (DFP)] in broiler diets were examined. The four diets contained up to 9 g calcium and 6 g phosphorus per kg and comparable energy and nutrient contents. Controls were fed a commercial diet with Ca-Na-phosphate as inorganic phosphorus source supplemented by phytase. In both fattening trials body weight gain, feed consumption and feed conversion were proved as well as the calcium and phosphorus levels in serum, the breaking strength of tibia or humerus and the femur mineralization (ash content in the fat free dry matter). Furthermore, in the balance trial the retention of calcium and phosphorus was determined by calculation (intake minus excretion) as well as by analysis of body composition. On a high performance level (that was only slightly influenced by the different treatments), the addition of DFP resulted in significantly reduced phosphorus availability (estimated by analysis of the whole carcass: control/MCP/DCP/DFP: 48.6/46.0/45.7/35.5%). The significantly reduced phosphorus level in serum (1.77 +/- 0.20/1.77 +/- 0.24/1.73 +/- 0.28 1.34 +/- 0.33 mmol/l) indicates the lower phosphorus retention in broilers given DFP. Furthermore, the crude ash content (582 +/- 17.6/580 +/- 18.6/563 +/- 15.2/547 +/- 29.7 g/kg fat free DM) and the breaking strength of bones (in right tibia in trial 2: 232 +/- 82.4/227 +/- 51.5/232 +/- 41.7/196 +/- 655 N) were lowest when given DFP. For diagnostic purposes it is of special interest that the phosphorus levels in the serum reflected markedly the different concentrations of available phosphorus in the diet.

Animal Feed↗
PubMed1975

Phosphorus depletion in children on long-term total parenteral nutrition.

The retention of nitrogen, calcium and phosphorus was studied in nine infants on total parenteral nutrition. The amounts of calcium, nitrogen and phosphorus were varied singly or simultaneously. The results demonstrate close interrelationships in the retention of these three elements. Not only the absolute amount of phosphorus perfused daily but also the amounts of nitrogen and/or calcium perfused simultaneously account for the phosphorus depletion that may lead to severe hypophosphatemia. The decrease in serum phosphorus concentration with a simultaneous fall of urinary phosphorus excretion to undetectable levels and a rise in urinary calcium output to 10 mg/kg/24 hours or more are warning symptoms of phosphorus depletion. Such a complication was observed in our first seven children on total parenteral nutrition. Phosphorus depletion can be prevented by using the following amounts of these elements in the perfusate: per 100 Kcal/kg/24 hours, 400 mg/kg/24 hours of nitrogen, 35 mg/kg/24 hours of calcium and 40 mg/kg/24 hours of phosphorus. With such a technique no phosphorus depletion was observed in any of the 63 subsequent patients whom we treated with total parenteral nutrition for periods varying from 20 days to 9 months.

Amino Acids↗
PubMed1996

Effect of aging on the metabolism of phosphorus and 1,25-dihydroxyvitamin D in healthy men.

We tested the hypothesis that aging alters physiological regulation of the serum concentration of 1,25-dihydroxyvitamin D [1,25(OH)2D] by inorganic phosphorus. In seven elderly men [age 71 +/- 1 (SE) yr] and 9 young men (29 +/- 2 yr), dietary phosphorus was first normal, then increased and decreased within its normal range. At each intake of phosphorus, serum concentrations of 1,25(OH)2D in the elderly did not differ from those in young men, but fasting and 24-h mean serum concentrations of phosphorus were lower in elderly men. With phosphorus restriction, in each group serum 1,25(OH)2D increased by 47%, and 24-h mean serum phosphorus decreased by 0.6 +/- 0.1 mg/dl. Serum concentrations of 1,25(OH)2D varied inversely with 24-h mean serum phosphorus (R= -0.92, P<0.0001). Thus, in healthy elderly men in whom glomerular filtration rate is normal or near normal, serum concentrations of 1,25(OH)2D increase when dietary phosphorus is restricted; the magnitude of response at steady state is unaffected by aging, but the time course of response is delayed. At any level of serum phosphorus, serum 1,25(OH)2D is lower than that in young men, as reflected by a lower intercept of regression of serum 1,25(OH)2D on 24-h mean phosphorus.

Adult↗
PubMed1989

Elevated Ca2+ does not inhibit the 1,25(OH)2D3 response to phosphorus restriction.

Phosphorus restriction and parathyroid hormone (PTH) are the most potent stimuli for 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] biosynthesis. Elevated arterial blood ionized calcium (Ca2+) inhibits the PTH-stimulated pathway for 1,25(OH)2D3 production. To determine whether the increase in Ca2+ due to chronic metabolic acidosis (CMA) would prevent stimulation of 1,25(OH)2D3 by dietary phosphorus restriction, rats were fed either a normal (NPD, 0.65%)- or low (LPD, 0.1%-phosphorus diet for 10 days. Ammonium chloride (NH4Cl) was added (1.5%) to the drinking water of some rats (CMA) while others served as nonacidemic controls. LPD increased serum 1,25(OH)2D3 levels in the absence of CMA and CMA did not affect the increase of 1,25(OH)2D3. LPD decreased serum phosphorus and increased Ca2+. Serum 1,25(OH)2D3 levels were correlated inversely with serum phosphorus and directly with Ca2+. Using stepwise linear regression the correlation between phosphorus and 1,25(OH)2D3 accounted for the majority of the variance contributed by both phosphorus and Ca2+ (F = 12.30, P less than 0.001). Increased Ca2+ induced by CMA does not inhibit the rise in serum 1,25(OH)2D3 during LPD, indicating that during phosphorus restriction Ca2+ does not inhibit production of 1,25(OH)2D3. Thus the mechanism whereby PTH and phosphorus restriction stimulate 1,25(OH)2D3 production differ; increased Ca2+ blocks the PTH-mediated rise in 1,25(OH)2D3 but does not alter the 1,25(OH)2D3 response to phosphorus restriction.

Ammonium Chloride↗
PubMedDate not supplied

A new graduated dosing regimen for phosphorus replacement in patients receiving nutrition support.

BACKGROUND: Hypophosphatemia is a common metabolic complication in patients receiving specialized nutrition support. We changed our previously reported dosing algorithm because the low dose no longer appeared to be effective at increasing serum phosphorus concentrations. The purpose of this study was to evaluate the safety and efficacy of a revised weight-based phosphorus-dosing algorithm in critically ill trauma patients receiving specialized nutrition support. METHODS: Seventy-nine adult trauma patients with hypophosphatemia (serum phosphorus concentration < or = 0.96 mmol/L) receiving nutrition support received an IV dose of phosphorus on day 1 according to the serum concentration of phosphorus: 0.73-0.96 mmol/L (0.32 mmol/kg, low dose), 0.51-0.72 mmol/L (0.64 mmol/kg, moderate dose), and < or = 0.5 mmol/L (1 mmol/kg, high dose). The IV phosphorus bolus dose was administered at 7.5 mmol/hour. Generally, patients with a serum potassium concentration <4 mmol/L received potassium phosphate and patients with a serum potassium concentration > or = 4 mmol/L received sodium phosphate. Patients who still had hypophosphatemia on day 2 were dosed using the new dosing algorithm by the nutrition support service according to that day's serum concentration of phosphorus, or empirically by the trauma service. RESULTS: Of the 79 patients studied, 57 were male and 22 were female with a mean age of 44.8 +/- 20.6 years. Mean Injury Severity Scores and APACHE-II scores were 27.1 +/- 11.6 and 15.2 +/- 6.8, respectively. There was no difference in baseline characteristics among the 3 dosing groups. Of the 79 patients, 34 received the low dose, 30 received the moderate dose, and 15 received the high dose of phosphorous. Mean serum phosphorous concentrations on day 2 were significantly increased in the moderate-dosed group (0.64 +/- 0.06 to 0.77 +/- 0.22 mmol/L, p < .05) and high-dosed group (0.38 +/- 0.06 to 0.93 +/- 0.32 mmol/L, p < .01), respectively, when compared with day 1. Mean serum phosphorus concentrations were normal in all 3 groups on day 3. Serum concentrations of magnesium, sodium, and potassium, as well as arterial pH, were stable across the study. Mean concentrations of ionized calcium were not significantly different in any of the 3 dosing groups across the study period. CONCLUSIONS: This weight-based phosphorus-dosing algorithm is safe for use in critically ill patients receiving nutrition support. The moderate and severe-dose regimens effectively increase serum phosphorus concentrations.

APACHE↗
PubMed1997

High phosphorus diet rapidly induces nephrocalcinosis and proximal tubular injury in rats.

The development of nephrocalcinosis and the time course of changes in kidney function, especially proximal tubular function, were studied in young male rats fed a high-phosphorus diet. The animals were fed a purified diet with a phosphorus content of either 0.5% (normal phosphorus diet) or 1.5% (high-phosphorus diet). In the group fed the high-phosphorus diet, nephrocalcinosis was found in 4 of 42 rats after 1 d of feeding and in all rats of this group at 3 d. The degree of nephrocalcinosis gradually increased with time. Upon histological observation by electron microscopy, vacuoles, lysosomes and swelling of microvilli in the proximal tubules were observed in rats fed the high-phosphorus diet after 1 d of feeding. Giant lysosomes with deposition of calcium and deposition of hydroxyapatite in mitochondria were observed in the proximal tubules of rats fed the high-phosphorus diet at 3 d. Albumin concentration in the urine of these rats was significantly increased at 3 d. The activity of N-acetyl-beta-D-glucosaminidase in the urine was also significantly increased after 1 d of feeding the high-phosphorus diet, and then reached a plateau. The beta 2-microglobulin concentration in the urine of rats fed the high-phosphorus diet was significantly increased at 14 d, and increased more toward 21 d. We concluded that nephrocalcinosis and injury to the proximal tubules are rapidly induced in rats fed a high-phosphorus diet.

Animals↗
PubMed1982

Dietary and plasma phosphorus in hens with fatty liver syndrome.

Plasma inorganic phosphorus was determined in two experiments in hens that had fatty liver syndrome. In Experiment 1, plasma inorganic phosphorus was determined in twelve strains of hens all fed the same diet. Plasma inorganic phosphorus immediately following oviposition was elevated in all strains. The two strains in the first experiment with the highest as well as the two strains with the lowest plasma inorganic phosphorus were used in the second experiment. Each of the four strains were subdivided into three groups of 60 hens each and fed a practical layer diet containing either .30, .75, or 1.40% total phosphorus and 3.4% calcium. Significant differences were found in plasma inorganic phosphorus between strains fed the three dietary phosphorus levels. Results indicated that plasma inorganic phosphorus is related to dietary phosphorus in hens with an elevated plasma inorganic phosphorus level associated with fatty liver syndrome.

Animals↗