Role of dietary phosphate restriction in chronic kidney disease.

AIM: Patients with progressive chronic kidney disease (CKD) develop positive phosphate balance that is associated with increased cardiovascular risk and mortality. Modification of dietary phosphate is a commonly used strategy to improve outcomes but is complicated by the need for adequate dietary protein. Surprisingly, the evidence for patient-level benefits from phosphate restriction is tenuous, and the justification for using any phosphate binder for pre-dialysis patients is questionable. METHODS: The evidence for dietary phosphate modification was reviewed, along with the possible role of a smart phone application (app) that provides information on phosphate, sodium, potassium and nutrients in over 50 000 Australian foods. A pilot study of healthy participants assigned to dietetic advice and standard diet sheets, or dietetic advice, diet sheets and use of the smart phone app was performed. RESULTS: Following baseline studies, 25 participants commenced the sodium and phosphate restricted diet. After 2 weeks, both groups showed non-significant trends to reduction in urinary phosphate and sodium. App users referred to information on the app more frequently than the control group participants referred to written instructions, found referring to the app more convenient, felt they learned more new information, were more motivated to maintain the diet and were more likely to recommend their information source to family or friends (all P < 0.05). CONCLUSIONS: Maintaining phosphate balance remains an important goal of CKD management, although diets incorporating very low phosphate and protein contents may worsen patient outcomes. For selected patients, a smart phone app may improve dietary acceptance and compliance.

Adiponectin alters renal calcium and phosphate excretion through regulation of klotho expression.

The kidney controls systemic calcium and phosphate levels and disturbances of its control mechanisms can lead to a variety of diseases. The insulin-sensitizing adipokine adiponectin is renoprotective and accelerates functional recovery following renal injury. However, unlike other adipokines, adiponectin is reduced in obesity. High adiponectin levels are also correlated with bone loss, suggestive of an additional action in mineral metabolism. Using knockout, wild-type, and adiponectin-overexpressing transgenic mice, we sought to identify the mechanistic basis for adiponectin's ability to regulate calcium and phosphate balance at the level of the kidney. Adiponectin knockout mice exhibited lower serum calcium, lower urinary calcium excretion, and markedly lower serum fibroblast growth factor 23 (FGF23) levels, although circulating klotho concentrations were significantly higher than in wild-type littermates. The transgenic mice exhibited lower bone mass and strength, particularly compared to adiponectin knockout mice. The transgenic mice were hyper-responsive to a 2% phosphate-enriched diet, exhibiting 2-fold higher serum FGF23 and concomitantly higher fractional phosphate excretion. These mice also excreted more calcium with calcium-enriched diet and had less renal klotho protein expression. In contrast, the knockout mice exhibited a smaller increase in FGF23 and maintained elevated klotho levels on both mineral challenges. Kidney-specific adiponectin expression in doxycycline-inducible adiponectin mice and adiponectin addition in vitro confirmed adiponectin's ability to reduce tubular epithelial cell klotho secretion. Thus, adiponectin alters calcium and phosphate balance and renal mineral excretion, in part, through klotho. This work highlights the profound effects of adipose tissue on renal function and has identified a new mechanism by which adiponectin may regulate bone mass.

Examining the Proportion of Dietary Phosphorus From Plants, Animals, and Food Additives Excreted in Urine.

Phosphorus bioavailability is an emerging topic of interest in the field of renal nutrition that has important research and clinical implications. Estimates of phosphorus bioavailability, based on digestibility, indicate that bioavailability of phosphorus increases from plants to animals to food additives. In this commentary, we examined the proportion of dietary phosphorus from plants, animals, and food additives excreted in urine from four controlled-feeding studies conducted in healthy adults and patients with chronic kidney disease. As expected, a smaller proportion of phosphorus from plant foods was excreted in urine compared to animal foods. However, contrary to expectations, phosphorus from food additives appeared to be incompletely absorbed. The apparent discrepancy between digestibility of phosphorus additives and the proportion excreted in urine suggests a need for human balance studies to determine the bioavailability of different sources of phosphorus.

The New Nordic Diet: phosphorus content and absorption.

PURPOSE: High phosphorus content in the diet may have adverse effect on cardiovascular health. We investigated whether the New Nordic Diet (NND), based mainly on local, organic and less processed food and large amounts of fruit, vegetables, wholegrain and fish, versus an Average Danish Diet (ADD) would reduce the phosphorus load due to less phosphorus-containing food additives, animal protein and more plant-based proteins. METHODS: Phosphorus and creatinine were measured in plasma and urine at baseline, week 12 and week 26 in 132 centrally obese subjects with normal renal function as part of a post hoc analysis of data acquired from a 26-week controlled trial. We used the fractional phosphorus excretion as a measurement of phosphorus absorption. RESULTS: Mean baseline fractional phosphorus excretion was 20.9 ± 6.6 % in the NND group (n = 82) and 20.8 ± 5.5 % in the ADD group (n = 50) and was decreased by 2.8 ± 5.1 and 3.1 ± 5.4 %, respectively, (p = 0.6) at week 26. At week 26, the mean change in plasma phosphorus was 0.04 ± 0.12 mmol/L in the NND group and -0.03 ± 0.13 mmol/L in the ADD group (p = 0.001). Mean baseline phosphorus intake was 1950 ± 16 mg/10 MJ in the NND group and 1968 ± 22 mg/10 MJ in the ADD group and decreased less in the NND compared to the ADD (67 ± 36 mg/10 MJ and -266 ± 45 mg/day, respectively, p < 0.298). CONCLUSION: Contrary to expectations, the NND had a high phosphorus intake and did not decrease the fractional phosphorus excretion compared with ADD. Further modifications of the diet are needed in order to make this food concept beneficial regarding phosphorus absorption.

Concordance of dietary sodium intake and concomitant phosphate load: Implications for sodium interventions.

BACKGROUND AND AIMS: Both a high dietary sodium and high phosphate load are associated with an increased cardiovascular risk in patients with chronic kidney disease (CKD), and possibly also in non-CKD populations. Sodium and phosphate are abundantly present in processed food. We hypothesized that (modulation of) dietary sodium is accompanied by changes in phosphate load across populations with normal and impaired renal function. METHODS AND RESULTS: We first investigated the association between sodium and phosphate load in 24-h urine samples from healthy controls (n = 252), patients with type 2 diabetes mellitus (DM, n = 255) and renal transplant recipients (RTR, n = 705). Secondly, we assessed the effect of sodium restriction on phosphate excretion in a nondiabetic CKD cohort (ND-CKD: n = 43) and a diabetic CKD cohort (D-CKD: n = 39). Sodium excretion correlated with phosphate excretion in healthy controls (R = 0.386, P < 0.001), DM (R = 0.490, P < 0.001), and RTR (R = 0.519, P < 0.001). This correlation was also present during regular sodium intake in the intervention studies (ND-CKD: R = 0.491, P < 0.001; D-CKD: R = 0.729, P < 0.001). In multivariable regression analysis, sodium excretion remained significantly correlated with phosphate excretion after adjustment for age, gender, BMI, and eGFR in all observational cohorts. In ND-CKD and D-CKD moderate sodium restriction reduced phosphate excretion (31 ± 10 to 28 ± 10 mmol/d; P = 0.04 and 26 ± 11 to 23 ± 9 mmol/d; P = 0.02 respectively). CONCLUSIONS: Dietary exposure to sodium and phosphate are correlated across the spectrum of renal function impairment. The concomitant reduction in phosphate intake accompanying sodium restriction underlines the off-target effects on other nutritional components, which may contribute to the beneficial cardiovascular effects of sodium restriction. (f) Registration numbers: Dutch Trial Register NTR675, NTR2366.

Consequences of a high phosphorus intake on mineral metabolism and bone remodeling in dependence of calcium intake in healthy subjects - a randomized placebo-controlled human intervention study.

BACKGROUND: Epidemiological studies reported an association between plasma phosphate concentrations and a higher risk for death and cardiovascular events in subjects free of chronic kidney diseases. The main aims of the present study were to determine the influence of a high phosphorus intake in combination with different calcium supplies on phosphorus, calcium, magnesium and iron metabolism as well as fibroblast growth factor 23 (FGF23) concentrations within eight weeks of supplementation. METHODS: Sixty-two healthy subjects completed the double-blind, placebo-controlled parallel designed study. Supplements were monosodium phosphate and calcium carbonate. During the first two weeks, all groups consumed a placebo sherbet powder, and afterwards, for eight weeks, a sherbet powder according to the intervention group: P1000/Ca0 (1 g/d phosphorus), P1000/Ca500 (1 g/d phosphorus and 0.5 g/d calcium) and P1000/Ca1000 (1 g/d phosphorus and 1 g/d calcium). Dietary records, fasting blood samplings, urine and fecal collections took place. RESULTS: Fasting plasma phosphate concentrations did not change after any intervention. After all interventions, renal excretions and fecal concentrations of phosphorus increased significantly after eight weeks. Renal calcium and magnesium excretion decreased significantly after eight weeks of P1000/Ca0 intervention compared to placebo. Plasma FGF23 concentrations were significantly higher after four weeks compared to eight weeks of all interventions. CONCLUSIONS: The long-term study showed in healthy adults no influence of high phosphorus intakes on fasting plasma phosphate concentrations. A high phosphorus intake without adequate calcium intake seems to have negative impact on calcium metabolism. Plasma FGF23 concentrations increased four weeks after high phosphorus intake and normalized after eight weeks. TRIAL REGISTRATION: The trial is registered at ClinicalTrials.gov as NCT02095392 .

Short communication: Individual cow variation in urinary excretion of phosphorus.

Some dairy cows excrete large amounts of P through their urine; thus, it was speculated that a genetic defect related to their efficiency in uptake of P or recirculation of P could cause such an effect. This speculation was pursued in a cross sectional study on 139 cows (103 Holstein and 36 Jersey) from an experimental herd using repeated sampling of urine (301 samples) to investigate sources of variation in urinary P concentration (Pu). Urine samples were taken on 6 testing sessions spread over 2 mo. Each sample was obtained by mild manual stimulation of the rear udder escutcheon area. The samples were immediately assayed for pH, stored frozen, and assayed for inorganic P and creatinine. Concentrations of P and creatinine in urine, the ratio of Pu to creatinine, and pH were analyzed using a linear mixed model. The model included fixed effects of breed, parity number, and sampling session. Stage of lactation was fitted as Wilmink-type lactation curves. Random effects included additive polygenic ancestry, permanent animal effects, and residual. The distribution of Pu approximated normality except for a single sample with very high Pu and very low pH. This sample came from a cow diagnosed independently with ketosis. For the remaining samples, it was shown that Pu has low to moderate heritability (0.12) and is only moderately repeatable (0.21). Based on a small data set, it is tentatively concluded that individual differences between cows exist in their Pu, and individual differences presumably result from genetic differences. However, it remains unclear if cows with genetically lower or higher Pu will perform better on a low-P diet.

Prediction of phosphorus output in manure and milk by lactating dairy cows.

Mathematical models for predicting P excretions play a key role in evaluating P use efficiency and monitoring the environmental impact of dairy cows. However, the majority of extant models require feed intake as predictor variable, which is not routinely available at farm level. The objectives of the study were to (1) explore factors explaining heterogeneity in P output; (2) develop a set of empirical models for predicting P output in feces (Pf), manure (PMa), and milk (Pm, all in g/cow per day) with and without dry matter intake (DMI) using literature data; and (3) evaluate new and extant P models using an independent data set. Random effect meta-regression analyses were conducted using 190 Pf, 97 PMa, and 118 Pm or milk P concentration (PMilkC) treatment means from 38 studies. Dietary nutrient composition, milk yield and composition, and days in milk were used as potential covariates to the models with and without DMI. Dietary phosphorus intake (Pi) was the major determinant of Pf and PMa. Milk yield negatively affected Pi partitioning to Pf or PMa. In the absence of DMI, milk yield, body weight, and dietary P content became the major determinants of Pf and PMa. Milk P concentration (PMilkC) was heterogeneous across the treatment groups, with a mean of 0.92 g/kg of milk. Milk yield, days in milk, and dietary Ca-to-ash ratio were negatively correlated with PMilkC and explained 42% of the heterogeneity. The new models predicted Pf and PMa with root mean square prediction error as a percentage of observed mean (RMSPE%) of 18.3 and 19.2%, respectively, using DMI when evaluated with an independent data set. Some of the extant models also predicted Pf and PMa well (RMSPE%=19.3 to 20.0%) using DMI. The new models without DMI as a variable predicted Pf and PMa with RMSPE% of 22.3 and 19.6%, respectively, which can be used in monitoring P excretions at farm level. When evaluated with an independent data set, the new model and extant models based on milk protein content predicted PMilkC with RMSPE% of 12.7 to 19.6%. Although models using P intake information gave better predictions, P output from lactating dairy cows can also be predicted well without intake using milk yield, milk protein content, body weight, and dietary P, Ca, and total ash contents.

The body composition and excretory burden of lean, obese, and severely obese individuals has implications for the assessment of chronic kidney disease.

Obesity could affect associations between creatinine generation, estimated body surface area, and excretory burden, with effects on chronic kidney disease assessment. We therefore examined the impact of obesity on the performances of estimated glomerular filtration rate (eGFR), the urine albumin:creatinine ratio (ACR), and excretory burden in 3611 participants of the Chronic Renal Insufficiency Cohort. Urine creatinine excretion significantly increased with body mass index (BMI) (34 and 31% greater at 40 kg/m(2) or more versus the normal of 18.5-25 kg/m(2)) in men and women, respectively, such that patients with a normal BMI and an ACR of 30 mg/g had the same 24-h albuminuria as severely obese patients with ACR 23 mg/g. The bias of eGFR (referenced to body surface area-indexed iothalamate (i-)GFR) had a U-shaped relationship to obesity in men but progressively increased in women. Nevertheless, obesity-associated body surface area increases were accompanied by a greater absolute (non-indexed) iGFR for a given eGFR, particularly in men. Two men with eGFRs of 45 ml/min per 1.73 m(2), height 1.76 m, and BMI 22 or 45 kg/m(2) had absolute iGFRs of 46 and 62 ml/min, respectively. The excretory burden, assessed as urine urea nitrogen and estimated dietary phosphorus, sodium, and potassium intakes, also increased in obesity. However, obese men had lower odds of anemia, hyperkalemia, and hyperphosphatemia. Thus, for a given ACR and eGFR, obese individuals have greater albuminuria, absolute GFR, and excretory burden. This has implications for chronic kidney disease management, screening, and research.

Phosphorus Intake and Potential Dietary Influences Examined via 24-Hour Urinary Biomarker Measurements in German Children and Adolescents Over 3 Decades.

BACKGROUND: Increases in phosphorus intake have been observed over the past years in adult populations. However, biomarker-based data are lacking on whether or not phosphorus intake also increased in children. OBJECTIVE: The aim of this study was to examine 24-hour urinary phosphate excretion (PO4-Ex) and diet-related biomarkers potentially influencing phosphorus status in German children and adolescents from 1985 to 2015. DESIGN: This longitudinal noninvasive biomarker-based cohort study examined 24-hour urine samples from children and adolescents of the Dortmund Nutritional and Anthropometric Longitudinally Designed Study, collected over 3 decades. PARTICIPANTS/SETTING: Examined individuals (n = 1,057) were healthy participants of the Dortmund Nutritional and Anthropometric Longitudinally Designed Study, situated in Dortmund, Germany, who had been asked to collect one yearly 24-hour urine sample. Six thousand seven hundred thirty-seven samples collected from participants aged 3 to 17 years between 1985 (baseline) and 2015, were included. MAIN OUTCOME MEASURES: phosphorus intake was examined biomarker-based by analyzed PO4-Ex in 24-hour urine samples. Whether acid-base status and intakes of protein, salt, and fruits and vegetables, may have relevantly contributed to PO4-Ex levels was assessed by determining 24-hour excretions of net acid, urea-nitrogen, and sodium as well as specific standardized excretions of potassium plus oxalate. STATISTICAL ANALYSES PERFORMED: Trend analysis over 30 years and potentially influencing diet factors were examined using linear mixed-effect regression models (PROC-MIXED). Adjustments for sex, age, and body surface area were performed. RESULTS: No change was identifiable for PO4-Ex over the 3 decades; neither in 3 to 8, 9 to 13, nor in 14 to 17 year olds. However, sodium excretion increased (P = .001). PROC-MIXED analysis on intraindividual changes in PO4-Ex revealed direct relationships with net acid excretion, urea-nitrogen, and sodium excretion and an inverse relationship with a biomarker of fruit and vegetable intake. CONCLUSIONS: Despite a direct relationship between PO4-Ex and a biomarker of industrially processed food consumption; that is, sodium excretion, which showed an increasing time trend, phosphorus intake was found to remain stable over decades in children and adolescents.

A new system of phosphorus and calcium requirements for lactating dairy cows.

Accurately predicting phosphorous (P) and calcium (Ca) dietary requirements is critical for optimizing dairy cattle performance, and minimizing mineral excretions and ecosystems eutrophication. This study provides a new factorial system to determine net and dietary P and Ca requirements for maintenance and lactation, derived from a meta-regression of mineral trials involving lactating dairy cows. A comprehensive global database was constructed from 57 peer-reviewed articles of mineral balance trials, with a wide range of dietary and animal performance data. We estimated the net requirements for maintenance from the intercept of a nonlinear equation between mineral intake and the sum of total fecal and urinary excretions, which is an estimate of endogenous mineral loss. Mineral secreted in milk was used to obtain net requirements for lactation. The mineral metabolizable coefficient was quantified through observed (treatment means) mineral intake and total fecal and urinary excretions, discounting the estimated endogenous excretions from our proposed models. The nonlinear models of total fecal and urinary mineral excretion were evaluated (observed versus predicted values) using a 5-fold cross validation approach. The models to estimate the sum of endogenous fecal and urinary excretions of P (0.135±0.043 g P/kg BW0.75) and Ca (0.360±0.144 g Ca/kg BW0.75) exhibited suitable precision and accuracy; r = 0.89 and 0.79, concordance correlation coefficient = 0.85 and 0.77, and root mean square prediction error = 24.1 and 20.5% observed means, respectively. Dietary variables (forage level, fiber, starch, crude protein, and ether extract) did not affect the metabolizable coefficient (MC) of P and Ca; therefore, an overall dietary MC of P (0.69±0.01) and Ca (0.65±0.02) were proposed. Our new system estimates lower net and dietary P requirements for lactating dairy cows compared to the NASEM-2021 and NRC-2001 models, but slightly higher Ca requirements than NASEM-2021.This proposed system holds potential to reduce the use of phosphorus in diets for dairy cows, and thus to enhance economic efficiency and environmental sustainability of the dairy industry.

The phosphate transporter NaPi-IIa determines the rapid renal adaptation to dietary phosphate intake in mouse irrespective of persistently high FGF23 levels.

Renal reabsorption of inorganic phosphate (Pi) is mediated by the phosphate transporters NaPi-IIa, NaPi-IIc, and Pit-2 in the proximal tubule brush border membrane (BBM). Dietary Pi intake regulates these transporters; however, the contribution of the specific isoforms to the rapid and slow phase is not fully clarified. Moreover, the regulation of PTH and FGF23, two major phosphaturic hormones, during the adaptive phase has not been correlated. C57/BL6 and NaPi-IIa(-/-) mice received 5 days either 1.2 % (HPD) or 0.1 % (LPD) Pi-containing diets. Thereafter, some mice were acutely switched to LPD or HPD. Plasma Pi concentrations were similar under chronic diets, but lower when mice were acutely switched to LPD. Urinary Pi excretion was similar in C57/BL6 and NaPi-IIa(-/-) mice under HPD. During chronic LPD, NaPi-IIa(-/-) mice lost phosphate in urine compensated by higher intestinal Pi absorption. During the acute HPD-to-LPD switch, NaPi-IIa(-/-) mice exhibited a delayed decrease in urinary Pi excretion. PTH was acutely regulated by low dietary Pi intake. FGF23 did not respond to low Pi intake within 8 h whereas the phospho-adaptator protein FRS2α necessary for FGF-receptor cell signaling was downregulated. BBM Pi transport activity and NaPi-IIa but not NaPi-IIc and Pit-2 abundance acutely adapted to diets in C57/BL6 mice. In NaPi-IIa(-/-), Pi transport activity was low and did not adapt. Thus, NaPi-IIa mediates the fast adaptation to Pi intake and is upregulated during the adaptation to low Pi despite persistently high FGF23 levels. The sensitivity to FGF23 may be regulated by adapting FRS2α abundance and phosphorylation.

Increased renal dopamine and acute renal adaptation to a high-phosphate diet.

The current experiments explore the role of dopamine in facilitating the acute increase in renal phosphate excretion in response to a high-phosphate diet. Compared with a low-phosphate (0.1%) diet for 24 h, mice fed a high-phosphate (1.2%) diet had significantly higher rates of phosphate excretion in the urine associated with a two- to threefold increase in the dopamine content of the kidney and in the urinary excretion of dopamine. Animals fed a high-phosphate diet had a significant increase in the abundance and activity of renal DOPA (l-dihydroxyphenylalanine) decarboxylase and significant reductions in renalase, monoamine oxidase A, and monoamine oxidase B. The activity of protein kinase A and protein kinase C, markers of activation of renal dopamine receptors, were significantly higher in animals fed a high-phosphate vs. a low-phosphate diet. Treatment of rats with carbidopa, an inhibitor of DOPA decarboxylase, impaired adaptation to a high-phosphate diet. These experiments indicate that the rapid adaptation to a high-phosphate diet involves alterations in key enzymes involved in dopamine synthesis and degradation, resulting in increased renal dopamine content and activation of the signaling cascade used by dopamine to inhibit the renal tubular reabsorption of phosphate.

Influence of high phosphorus intake on salivary and plasma concentrations, and urinary phosphorus excretion in mature ponies.

This study addressed the question whether the concentration of phosphorus (P) in saliva of ponies is influenced by P intake. Six ponies were fed a diet high in P (HP treatment), providing 21 g P/day, and a diet low in P (LP treatment), supplying 7 g P/day. The two diets provided approximately 21 g calcium (Ca) and 6 g magnesium (Mg)/day. The experiment had an A-B-A design with treatment periods of 30 days. The ponies first received the HP diet (HP1), followed by the LP treatment and were then fed again the HP diet (HP2). Urinary P excretion was increased in both HP feeding periods and equalled approximately 7% of P intake vs. 0.5% on the LP diet. Plasma P concentration was higher for the HP treatment. The salivary P concentration ranged from 0 to 1.01 mmol P/l between ponies and there was no effect of P intake. It is suggested that saliva is not an important excretion route of P. The percentage of Ca and Mg in urine (% of intake) was higher for the LP treatment than for the HP treatments. The results of this study suggest that salivary Mg may contribute to Mg homeostasis.

Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency.

Dietary potassium (K) deficiency is accompanied by phosphaturia and decreased renal brush border membrane (BBM) vesicle sodium (Na)-dependent phosphate (P(i)) transport activity. Our laboratory previously showed that K deficiency in rats leads to increased abundance in the proximal tubule BBM of the apical Na-P(i) cotransporter NaPi-IIa, but that the activity, diffusion, and clustering of NaPi-IIa could be modulated by the altered lipid composition of the K-deficient BBM (Zajicek HK, Wang H, Puttaparthi K, Halaihel N, Markovich D, Shayman J, Beliveau R, Wilson P, Rogers T, Levi M. Kidney Int 60: 694-704, 2001; Inoue M, Digman MA, Cheng M, Breusegem SY, Halaihel N, Sorribas V, Mantulin WW, Gratton E, Barry NP, Levi M. J Biol Chem 279: 49160-49171, 2004). Here we investigated the role of the renal Na-P(i) cotransporters NaPi-IIc and PiT-2 in K deficiency. Using Western blotting, immunofluorescence, and quantitative real-time PCR, we found that, in rats and in mice, K deficiency is associated with a dramatic decrease in the NaPi-IIc protein abundance in proximal tubular BBM and in NaPi-IIc mRNA. In addition, we documented the presence of a third Na-coupled P(i) transporter in the renal BBM, PiT-2, whose abundance is also decreased by dietary K deficiency in rats and in mice. Finally, electron microscopy showed subcellular redistribution of NaPi-IIc in K deficiency: in control rats, NaPi-IIc immunolabel was primarily in BBM microvilli, whereas, in K-deficient rats, NaPi-IIc BBM label was reduced, and immunolabel was prevalent in cytoplasmic vesicles. In summary, our results demonstrate that decreases in BBM abundance of the phosphate transporter NaPi-IIc and also PiT-2 might contribute to the phosphaturia of dietary K deficiency, and that the three renal BBM phosphate transporters characterized so far can be differentially regulated by dietary perturbations.

Dietary phosphorus intake estimated by 4-day dietary records and two 24-hour urine collections and their associated factors in Japanese adults.

BACKGROUND/OBJECTIVES: Both self-reported dietary information and urinary excretion have limitations in the assessment of phosphorus intake. We conducted a cross-sectional study to estimate dietary phosphorus intake by dietary records (DR) and 24-h urine collections (UC) and examined associated factors. SUBJECTS/METHODS: A total of 161 men and 161 women aged 20-69 years completed a 4-day DR and two 24-h UC. Phosphorus intake by UC was estimated using the mean phosphorus absorption rate of 14 papers. Associations between phosphorus intake and urinary excretion and age, body mass index (BMI), physical activity, education, and smoking status were examined using multiple linear regression. RESULTS: Phosphorus intake estimated by UC was higher than that estimated by DR (mean: 1393 vs. 1176 mg/day, P < 0.0001 in men; 1082 vs. 1021 mg/day, P = 0.008 in women). Values were significantly correlated (r = 0.29, P = 0.0002 in men; r = 0.30, P = 0.0001 in women). Phosphorus intake estimated by DR was positively associated with age in women. Male current smokers consumed less phosphorus than never smokers. Higher urinary phosphorus excretion was associated with higher BMI in both sexes and higher physical activity in women. CONCLUSIONS: This study showed dietary phosphorus intakes estimated by 4-day DR and by 2-day UC in adults. Although dietary phosphorus intake estimated by DR showed moderate correlation with that by UC, they differed in their association with age, BMI, physical activity, and smoking status.

Effect of different concentrations of dietary P and Ca on plasma inorganic P and urinary P excretion using noncolostomized and colostomized broilers.

Two 5-d bioassays were conducted to explore the P physiological threshold in broilers based on plasma inorganic P (iP), urinary P and Ca, and excreta P and Ca measurements in non-colostomized and colostomized broilers fed with different concentrations of non-phytate P (NPP) and Ca. In Experiment 1, 80 40-day-old Cobb 500 non-colostomized male broilers were assorted into 8 groups consisting of 10 broilers each and placed in individual metabolic cages. Similarly, 8 colostomized broilers of same age were allotted to 8 individual metabolic cages. The experimental diets consisted of a corn soybean meal basal containing 0.17% phytate P (PP) with 8 concentrations (0.08, 0.13, 0.18, 0.23, 0.28, 0.33, 0.38, and 0.45%) of NPP. The dietary Ca concentration was maintained at 0.5% by adjusting a 185-micron particle size limestone with each concentration of added P from added calcium phosphate, dibasic, monohydrate. After Experiment 1, broilers were fed a standard grower diet for 5 d and Experiment 2 was conducted the same as Experiment 1; however, Ca was maintained at 0.9% for all test diets. Plasma iP, urinary P and Ca, and total P (TP) and Ca retention along with phytate P hydrolysis were measured. At 0.5% Ca dietary level, the inflection points for dietary NPP obtained from segmented line regression analysis for plasma iP, urinary P, and urinary Ca were 0.26% (±0.04 SE), 0.28% (±0.01 SE), and 0.30% (±0.04 SE), respectively. The similar values for 0.9% Ca diets were 0.27% (±0.03 SE), 0.21% (±0.03 SE), and 0.30% (±0.0 SE), respectively. In summary, the present findings suggest that an increased dietary NPP would increase plasma inorganic P concentration along with increased % retention of TP and NPP until the broilers reach a point of physiological steady state (7.51 mg iP/dL - 8.13 mg iP/dL as found in this study). Excess P beyond physiological threshold is eliminated in urine coupled with decreased % retention.

Calcium particle size effects on plasma, excreta, and urinary Ca and P changes in broiler breeder hens.

An experiment was conducted using non-colostomized and colostomized broiler breeder hens to determine the effects of feeding limestone of 2 different mean particle sizes (185 microns and 3490 microns) on P excretion, total P and Ca retention, and urinary P and Ca excretion during a 6-week feeding study. Additionally, changes in plasma inorganic P (iP) and ionic Ca (Ca++) and urinary excretion of P and Ca were determined in one egg laying cycle of 24 hours. One-hundred-fifty non-colostomized and 6 colostomized broiler breeder hens, 30 wk of age, were divided into 2 groups and fed broiler breeder diets supplemented with either small particle or large particle limestone. Two % acid insoluble ash (Celite) was added to the feed as a marker. Diets, excreta, and urine samples were analyzed for total P and Ca by ionic coupling plasma (ICP) analysis. The non-colostomized breeders fed large particle limestone compared to small limestone particles produced a significant increase in percent tibia ash (P < 0.0001) and egg specific gravity (P = 0.0382), but P excretion approached a tendency of being reduced (P = 0.1585). The urinary total P and Ca (∼18 and 9%, respectively) of total P and Ca excretion for breeders fed both sizes of limestone was not significantly different in the colostomized breeders. In plasma, both iP and Ca++ reached a peak during 18 to 20 h and 20 to 24 h post oviposition for smaller and larger particle sized limestone fed groups, respectively. The maximal excretion of urinary P was found during 11 to 20 h post oviposition, whereas urinary Ca peaked during 0 to 11 h post oviposition for both smaller and larger particle sized limestone supplemented groups. In summary, the findings indicate that the particle size (smaller and larger) of calcium source did not significantly influence the quantitative total urinary excretion of Ca and P but did influence the timing of Ca and P excretion.

Habitual dietary phosphorus intake and urinary excretion in chronic kidney disease patients: a 3-day observational study.

Hyperphosphatemia in chronic kidney disease (CKD) is associated with vascular calcification, cardiovascular morbidity and mortality. The aim of this study was to estimate the daily dietary phosphorus intake compared with recommendations in CKD patients and to evaluate the reproducibility of the 24-h urinary phosphorus excretion. Twenty CKD patients stage 3-4 from the outpatient clinic, collected 24-h urine and kept dietary records for 3 consecutive days. The mean daily phosphorus intake was 1367±499, 1642±815 and 1426±706 mg/day, respectively (P=0.57). The mean urinary phosphorus excretion was 914±465, 954±414 and 994±479 mg/day, respectively (P=0.21). In this population of CKD patients stage 3-4 the daily phosphorus intake was above the recommended. Twenty-four-hour urinary phosphorus excretion was reproducible and the data indicate that a single 24-h urine collection is sufficient to estimate the individual phosphorus excretion.

Quantitative relationships between standardized total tract digestible phosphorus and total calcium intakes and their retention and excretion in growing pigs fed corn-soybean meal diets.

An experiment was conducted to determine the quantitative relationships between standardized total tract digestible P (STTD P) and total Ca intakes with their retention and excretion by growing pigs fed corn-soybean meal diets. Forty-eight crossbred barrows (BW = 22.7 ± 2.9 kg) were allotted to 1 of 8 diets, housed individually in pens for 3 wk, and then moved to metabolism crates and allowed 4 d for adaptation and 5 d for collection of urine and fecal samples. Eight corn-soybean meal diets were formulated for similar NE, fat, and AA concentrations but to increase the STTD P from 0.16 to 0.62% using monocalcium phosphate. Dietary treatments were formulated for a constant Ca:STTD P ratio (2.2:1). The STTD P intake increased (P < 0.001) from 64 to 242% of the daily requirement (4.59 g/d of STTD P). Fecal and total excretion of P and Ca were linearly associated with mineral intake (P < 0.001). Constant urinary P excretion of 0.03 g/d P was observed, but at 4.96 g/d of STTD P intake, the urinary P excretion increased (P < 0.001). In contrast, Ca excretion in urine decreased (P < 0.001) with Ca intake, but constant excretion of 0.40 g/d Ca was reached at 17.97 g/d of Ca intake. The daily intakes of STTD P and Ca moderately explained the variation in urinary excretion of P (R2= 0.41) and Ca (R2= 0.64). The absorption and retention of P increased linearly (P< 0.001) with dietary P intake, whereas absorption and retention of Ca showed a quadratic response (P < 0.001). Absorption and retention of P and Ca were highly predictable from the STTD P and Ca intakes, with of 0.87 and 0.90, respectively. The femur mineral content (FMC) increased by 2.71 g with STTD P intake (P < 0.001) but reached a plateau (29.54 g of FMC) at 8.84 g/d of STTD P intake. The FMC was highly predictable from the STTD P intake (R2 = 0.89). The FMC affected the urinary P excretion ( P< 0.01), but moderately (R2= 0.19) explained the variation in urinary P. In conclusion, constant excretion of P in urine was observed but excretion increased linearly at STTD P intake levels above the requirement for maximum growth of growing pigs. The FMC increased with STTD P intake, but a plateau was reached at a STTD P intake level above the requirement. Dietary STTD P was used for growth and accumulated in bones until a plateau was reached and excess was excreted in urine. The predictability of P and Ca excretion in urine from the dietary STTD P and Ca intakes was moderate.