Urinary phosphorus excretion in fish: environmental and aquaculture implications

Urinary and faecal phosphorus excretion were measured in five sheep for 4 days after acute intravenous infusion of 3.38 g of phosphorus as potassium dihydrogen phosphate. Urinary phosphorus excretion was increased for 12 hr after the infusion, but urinary phosphorus output was small compared with the marked increase in faecal phosphorus output. The increase in faecal phosphorus excretion coincided with and followed the appearance in the faeces of Cr-EDTA, which had been introduced into the rumen as a marker at the time of the phosphate infusion. This suggests that secretion of phosphorus into gut regions below the reticulo-rumen is not quantitatively altered in response to intravenous phosphorus loading, and that phosphorus absorption is also unaffected (at least not on a short-term basis). The additional phosphorus entered the alimentary canal at the level of the reticulo-rumen, and it was deduced that this occurred predominantly via the salivary glands. Persistence of the increase in faecal phosphorus excretion for some time after the Cr-EDTA marker had been cleared emphasizes the importance of the phosphorus recirculation system to ruminants like the sheep.

Urinary phosphorus excretion by sheep given diets of coarse or finely ground roughage to vary their salivary flow rates, was studied. A 3 x 3 Latin square design was used in which three Merino ewes with rumen fistulas were given nutritionally complete diets in which the roughage component consisted of oat hulls (diet A), finely ground oat hulls (0.8 mm screen) (diet B), and finely ground oat hulls with added polyethylene flakes (diet C). Daily rumination time was used as an index of relative saliva flow rate and varied from 7.59?0 .47 and 6.83?1.12 hr/day for diets A and C respectively, to 1.92?0.39 hr/day for diet B. Similar changes were observed for the daily number of chews. When the sheep were given diet B, the pH of the rumen fluid, the concentration of inorganic phosphorus in the rumen fluid and the total inorganic phosphorus content of the rumen were reduced relative to diets A and C. Each of these effects points to a reduced rate of saliva flow. The inorganic phosphorus levels of the plasma were unaffected by the dietary treatments except that in the 6 hr following feeding, the levels fell for treatments A and C, but rose for treatment B. Urinary phosphorus excretion, which was significantly increased by diet B, was 356.6, 472.7 and 373.5 mg/day for diets A, B and C respectively. Urinary and faecal excretions of phosphorus were significantly correlated (r = –0.86) as were the urinary excretion and rumen content of phosphorus (r = –0.88). The data are discussed in relation to the role of salivary secretion of phosphorus in the balance between faecal and urinary excretion of phosphorus in sheep. _________________ *Part I, Aust. J. Agric. Res., 25: 475-83 (1974).

Disorders of mineral metabolism are more common in African Americans with CKD than in European Americans with CKD. Previous studies have focused on the differences in mineral metabolism by self-reported race, making it difficult to delineate the importance of environmental compared with biologic factors. In a cross-sectional analysis of 3013 participants of the Chronic Renal Insufficiency Cohort study with complete data, we compared markers of mineral metabolism (phosphorus, calcium, alkaline phosphatase, parathyroid hormone, fibroblast growth factor 23, and urine calcium and phosphorus excretion) in European Americans versus African Americans and separately, across quartiles of genetic African ancestry in African Americans (n=1490). Compared with European Americans, African Americans had higher blood concentrations of phosphorus, alkaline phosphatase, fibroblast growth factor 23, and parathyroid hormone, lower 24-hour urinary excretion of calcium and phosphorus, and lower urinary fractional excretion of calcium and phosphorus at baseline (P<0.001 for all). Among African Americans, a higher percentage of African ancestry was associated with lower 24-hour urinary excretion of phosphorus (Ptrend<0.01) in unadjusted analyses. In linear regression models adjusted for socio-demographic characteristics, kidney function, serum phosphorus, and dietary phosphorus intake, higher percentage of African ancestry was significantly associated with lower 24-hour urinary phosphorus excretion (each 10% higher African ancestry was associated with 39.6 mg lower 24-hour urinary phosphorus, P<0.001) and fractional excretion of phosphorus (each 10% higher African ancestry was associated with an absolute 1.1% lower fractional excretion of phosphorus, P=0.01). A higher percentage of African ancestry was independently associated with lower 24-hour urinary phosphorus excretion and lower fractional excretion of phosphorus among African Americans with CKD. These findings suggest that genetic variability might contribute to racial differences in urinary phosphorus excretion in CKD.

To study the effects of diabetes on the renal actions of parathyroid hormone (PTH), we observed urinary excretion of cyclic adenosine monophosphate (cAMP) and phosphorus in isolated perfused rat kidney. Diabetic rats were kept for 7 days after an intraperitoneal injection of 70 mg/kg streptozotocin (STZ). STZ-induced diabetic rats were treated with a daily injection of 20 U/kg lente-type insulin for 7 days. Plasma albumin, calcium, phosphorus, and PTH levels were not different among normal control, diabetic and insulin-treated diabetic groups. In the control rat kidney, the addition of PTH increased urinary cAMP excretion from 8 +/- 3 to 190 +/- 49 pmol/5 min and urinary phosphorus excretion from 11.3 +/- 4.4 to 33.6 +/- 10.8 microg/5 min. In the STZ-diabetic rat kidney, basal urinary cAMP was impaired, and PTH altered neither urinary cAMP nor phosphorus excretion (from below 0.7 to below 0.7 pmol/5 min, and from 15.5 +/-4.5 to 13.6 +/- 8.1 microg/5 min, respectively). Insulin treatment completely recovered the PTH actions. These results show that insulinopenic diabetes induces PTH resistance in the kidney.

Acid Load and Phosphorus Homeostasis in CKD

To determine the effect of continuous IV administration of 50% dextrose solution on phosphorus homeostasis in lactating dairy cows. Clinical trial. 4 multiparous Jersey cows. Cows were administered 50% dextrose solution IV (0.3 g/kg/h [0.14 g/lb/h]) for 5 days. Plasma concentrations of glucose, immune-reactive insulin (IRI), and phosphorus were determined before, during, and for 72 hours after dextrose infusion. Phosphorus intake and losses of phosphorus in urine, feces, and milk were determined. Each cow received a sham treatment that included instrumentation and sampling but not administration of dextrose. Plasma glucose, IRI, and phosphorus concentrations were stable during sham treatment. Plasma phosphorus concentration decreased rapidly after onset of dextrose infusion, reaching a nadir in 24 hours and remaining less than baseline value for 36 hours. Plasma phosphorus concentration increased after dextrose infusion was stopped, peaking in 6 hours. Urinary phosphorus excretion did not change during dextrose infusion, but phosphorus intake decreased because of reduced feed intake, followed by decreased fecal phosphorus loss and milk yield. Rapid changes in plasma phosphorus concentration at the start and end of dextrose infusion were temporally associated with changes in plasma glucose and IRI concentrations and most likely caused by compartmental shifts of phosphorus. Hypophosphatemia developed in response to hyperglycemia or hyperinsulinemia in dairy cows administered dextrose via continuous IV infusion. Veterinarians should monitor plasma phosphorus concentration when administering dextrose in this manner, particularly in cows with decreased appetite or preexisting hypophosphatemia.

The Percentage of Dietary Phosphorus Excreted in the Urine Varies by Dietary Pattern in a Randomized Feeding Study in Adults

The objective of the present study was to develop prediction equations for daily phosphorus excretion based on body weight (BW) and dietary phosphorus concentration of pigs. Four experiments were conducted using pigs with an initial body weight of 15 kg, 30 kg, 50 kg, and 78 kg. In the experiment 1, the experimental diets were mainly based on corn, soybean meal, whey powder, fish meal, and blood plasma. In the experiments 2, 3, and 4, the diets based on corn, soybean meal, and fibrous ingredients were formulated. All experimental diets were supplemented with commercial phytase at 500 FTU/kg. In all experiments, a total collection method and the marker-to-marker procedure were used for fecal and urinary collection. Fecal and urinary phosphorus excretions were determined. Correlation coefficients among BW, daily phosphorus intake, and daily phosphorus excretion of pigs were determined. Prediction equations for phosphorus excretion were developed using BW and dietary phosphorus concentration as independent variables. The BW had positive correlations with fecal and total phosphorus excretion (r = 0.78 and P &amp;lt; 0.001 for fecal phosphorus excretion and r = 0.78 and P &amp;lt; 0.001 for total phosphorus excretion). The prediction equations for predicting fecal phosphorus excretion and total phosphorus excretion were: fecal phosphorus excretion (g·pig–1·d–1) = –0.647 – 0.00065 × BW2 + 0.270 × BW × dietary phosphorus concentration (R2 = 0.81; P &amp;lt; 0.001); total phosphorus excretion (g·pig–1·d–1) = –0.619 – 0.00064 × BW2 + 0.277 × BW × dietary phosphorus concentration (R2 = 0.85; P &amp;lt; 0.001) where BW in kg and phosphorus concentration in %. The BW of pigs corresponding to the age was predicted using the NRC model. The mean phosphorus excretion of pigs weighing from 7 kg to 120 kg at day 22 to 180 was calculated using a developed estimation equation, with BW and total phosphorus requirement used as independent variables. Daily fecal and total phosphorus excretions were 3.77 g·pig–1·d–1 and 4.01 g·pig–1·d–1, respectively.

The metabolism of calcium and phosphorus in mature sheep, given firstly a chaff diet and then chaff with an intravenous supplement of 1.5-2.0 g/day of phosphorus, was studied by using tracer techniques and compartmental analysis. Absorption was also studied by deconvolution analysis and a technique relating the excretion of tracer in faeces to that of an insoluble marker. Under the conditions of the experiment most of the additional phosphorus infused intravenously was excreted in the faeces, and this was due to a concurrent increase in the endogenous secretion and a decrease in the efficiency of absorption of phosphorus. In sheep given 2.0 g of phosphorus per day, the phosphorus concentration in plasma increased 2.5-4 times, but the excretion of phosphorus in the urine remained small (less than 0.3 g/day) compared with the excretion of 2.5 g/day of phosphorus in the faeces. One feature of the experiment was the difference in the behaviour of bone and soft tissue reservoirs between the sheep given 1.5 g/day of phosphorus and those given 2.0 g/day. In the former group accretion and resorption of calcium and phosphorus in bone and soft tissue increased when compared with the control period, whereas in the latter group bone and soft tissue accretion of phosphorus was unchanged and resorption increased slightly. These results are discussed in terms of the hormonal changes that occur following changes in plasma calcium and phosphorus.

The control of phosphorus excretion in sheep has been examined by constructing a kinetic model that contains a mechanistic set of connections between blood and gastrointestinal tract. The model was developed using experimental data from chaff-fed sheep and gives an accurate description of the absorption and excretion of phosphorus in feces and urine of the ruminating sheep. Simulation of the response to an intravenous phosphorus infusion by adding an inflow of 2 g/day of phosphorus into the compartment describing blood, predicted values for fecal output of phosphorus lower than found experimentally. However, by alteration of the parameters describing absorption or salivation, the predictions approached experimental values. Similarly simulation of the conditions existing when a liquid diet was infused directly into the abomasum, i.e., a decrease in salivation rate [L(4.1)] and dietary phosphorus entering compartment 5 (abomasum) instead of compartment 4 (rumen), gave incorrect predictions for plasma and urinary phosphorus, but when the parameter for urinary phosphorus was increased the predicted values approached experimental values. These results indicated the main control site for phosphorus excretion in the ruminating sheep was the gastrointestinal tract, whereas for the nonruminating sheep fed the liquid diet, control was exerted by the kidney. A critical factor in the induction of adaptation of phosphorus reabsorption by the kidney was the reduction in salivation, and since this response occurred independently of marked changes in the delivery of phosphorus to the kidney, a humoral factor may be involved in this communication between salivary gland and kidney.

Association of urinary calcium and phosphorus excretion with renal disease progression in type 2 diabetes

Calcium, magnesium and phosphorus balance of sows during lactation for three parities

Background. The endogenous way of caries prevention plays a much greater role during the period of formation of hard tissues of teeth than during the period of teeth that have already formed. The endogenous prevention allows to have a higher level of caries resistance in the future. The use of calcium and phosphorus preparations as part of caries prevention programs is recognized as one of the most effective ways to prevent this pathology. Inorganic phosphorus-calcium preparations, which are introduced into the cariogenic diet contribute to the reduction of dental caries [15, 16]. Purpose – the aim of our study was to research calcium-phosphorus metabolism in young children against the background of connective tissue dysplasia. Materials and methods. At the dispensary observation were 39 children (the main group) aged 1 year and 2 months up to 3 years old with multiple caries and with complicated forms of caries against the background of genetically determined connective tissue pathology. The control group consisted of children without somatic pathology (healthy), with caries and with complicated forms of caries, their number was 35 children. These children of the main group were diagnosed with connective tissue dysplasia by doctors and geneticists. All children were divided into four groups, depending on age. The 1st group included 7 children aged 14 to 18 months; in the 2nd – 8 children aged 19 to 23 months; in the 3rd – 7 children aged 24 to 29 months, and in the 4th – 17 children aged 30 to 36 months. So, the largest group (17 people) consisted of children aged 30 to 36 months. Children were subjected to biochemical tests of blood and urine for the content and excretion of calcium and phosphorus. Results and their discussion. As a result of the conducted research, it was established that the level of calcium and phosphorus in the blood of children in all age groups is as follows: the level of calcium in the blood of children aged 14–18 months in the control group was 2.31 ± 0.07, in the main group – 2.42 ± 0.14. the level of calcium in the blood of children aged 19–23 months in the control group was 2.31 ± 0.08, in the primary – 2.41 ± 0.11, the level of calcium in the blood of children aged 24–29 months in the control group was 2.39 ± 0.10, in the main group – 2.35 ± 0.12, the level of calcium in the blood of children aged 30–36 months in the control group – 2.32 ± 0.11, in the main group – 2.35 ± 0.07. As a result of research conducted on children of the control and main groups aged from 14 to 30 months, we obtained data that correspond to the physiological norm (the content of Ca in the blood is within the norm – 2.20–2.70 mmol/l, the content of P in the blood – 1.45–1.78 mm/l). To characterize the state of phosphorus metabolism, it is necessary to take into account the ratio of the amount of calcium and phosphorus in blood serum and urine. Unused phosphorus is excreted in the urine. Excess calcium is excreted from the body with urine. Thus, in our opinion, the appointment of calcium and phosphorus preparations for the purpose of secondary endogenous prevention in young children with diseases of the hard tissues of the teeth against the background of genetically determined pathology of the connective tissue is not appropriate, because the concentration of calcium and phosphorus in the urine is reduced. Conclusions. When conducting endogenous prophylaxis in young children with genetically determined connective tissue pathology, it is necessary to take into account the level of calcium and phosphorus in the urine.

To examine whether lanthanum carbonate can induce a low phosphorus status in experimental animals, we examined phosphorus balance in rats administered lanthanum carbonate. Male 8-week-old Wistar rats were fed a basal case-in-based semi-purified diet or the basal diet supplemented with 0.45% or 0.90% lanthanum as lanthanum carbonate for 4 weeks. Lanthanum administration did not influence body or several organ weights and liver function. In rats administered lanthanum, a very small quantity of lanthanum was detected in several organs although the apparent absorption was almost zero. The highest lanthanum concentration was observed in the liver followed by the femur and kidney. Lanthanum was not clearly detected in the brain. Differences in organ lanthanum between 0.45% and 0.90% administration groups were not significant; lanthanum accumulation in the body is very low and may reach a plateau in a certain range of intake. Serum phosphorus was decreased and fecal phosphorus was increased by lanthanum administration dose-dependently. Urinary phosphorus excretion was significantly decreased by lanthanum. Since urinary phosphorus of rats fed 0.45% lanthanum diet decreased to near zero, the highest phosphorus balance was observed in rats fed 0.45% lanthanum diet. This high balance is considered to be adaptation to the low phosphorus status induced by lanthanum carbonate. These results indicate that lanthanum carbonate can induce hypophosphatemia without any direct side effects and be used to examine the effect of removing phosphorus from the diet in animal nutritional studies.

This study determined the specific reference values for urinary phosphorus excretion in healthy children and adolescents aged 2-18 years and evaluated whether they changed with age during growth and were gender dependent. We enrolled 3913 healthy children and adolescents aged 2-18 years to this study. The study population was divided into age groups, and the analysis was performed in one-year periods, separately for boys and girls. Urinary phosphorus excretion was analysed using four categories: P1 in mmol/24 hour units, P2 in mmol/kg/24 hours, P3 in mmol/1.73 m2 /24 hours and P4 in mmol/mmol creatinine. Clear differences in urinary exertion for girls and boys were observed as well as systematic changes with age. The boys presented with significantly higher daily urinary phosphorus excretion independent of its manner of expression (p < 0.001). The median urinary phosphorus (P1) rose with age (p < 0.001). Percentile tables of phosphorous exertion are presented. This was the largest study of urinary phosphate excretion based on a randomly selected sample of girls and boys aged 2-18 years. It highlights the importance of determining phosphorus reference values for children of different ages to provide early diagnosis and treatment for urolithiasis.