Evaluation of calcium to phosphorus ratio in spot urine samples as a practical method to monitor phosphorus intake adequacy in sows

The objective of this study was to evaluate the reliability of using Ca to P ratio measured in spot urine samples to assess P intake adequacy in gestating and lactating sows. A total of 36 sows were fed one of six concentrations of dietary total P (0.40, 0.48, 0.56, 0.64, 0.72, 0.80%) from day 7.5 + 1 after breeding until the end of lactation (day 26.6 + 1). Dietary Ca to P ratio was maintained constant across treatments at 1.25. Total 24-hour urine samples were collected in mid and late gestation (days 77.1 + 2 and 112.4 + 1), and early and late lactation (days 4.5 + 1 and 18.2 + 1). In parallel to 24-hour collections, spot urine samples were collected at three different times (early morning, late morning, and late afternoon) in late gestation and late lactation. Urine Ca and P concentrations were measured and Ca to P ratio was calculated. Sows were classified as P-adequate or P-deficient according to dietary P intake. Urine Ca to P ratio was greater in sows fed P-deficient diets than sows fed P-adequate diets (P < 0.001). Receiver operator characteristic (ROC) curves were used to determine the cut-off values for urine Ca to P ratio to predict P intake adequacy. Three different categories of P intake were defined according to urine Ca to P ratio: deficient, adequate, and excessive. The area under the ROC for Ca to P ratio was 0.88 (95% CI 0.81 – 0.95). Best cut-off value of urine Ca to P ratio was 1.5 (sensitivity 94% and specificity 68%) to identify sows fed P-deficient diets and 0.5 for P-excessive diets (sensitivity 82% and specificity 82%). A strong relationship between Ca to P ratio in 24-hour and spot urine samples was determined (r = 0.93, P < 0.01), independent of physiological state and collection time of spot samples (adjusted-R 2 = 0.86, P < 0.01). The degree of agreement between spot and 24-hour urine for P intake adequacy, assessed by Cohen’s weighted kappa analysis, was substantial (0.78, 95% CI 0.69 – 0.88). We conclude that urinary Ca to P ratio provides a reliable prediction of the adequacy of P intake in reproducing sows. Urinary Ca to P ratio measurements in random spot urinary offers a practical method to determine dietary P adequacy.

Mineral Balance and Metabolic Syndrome in Adolescents: Focus on Calcium and Phosphorus Intake

The incidence of metabolic syndrome, a chronic disease, tends to increase in adolescence, but has not been a high priority in delivery of health services. This study was to investigate the relationship between metabolic syndrome prevalence and mineral balance such as calcium and phosphorus intake among Korean adolescents. This study is a cross-sectional descriptive study using data from the 7th Korean national health and nutrition examination survey (KNHANES) VII-3 (2018) and the 8th KNHANES VII-1 (2019). A total of 895 adolescents aged 12 to 18 who filled in mineral intake questionnaires were analyzed using SPSS. According to their responses, only 2.9% of the subjects had a calcium: phosphorus intake ratio of 1:1, which is the recommended ratio. Daily phosphorus intake was significantly correlated with systolic blood pressure (r = 0.448, p < 0.001), waist circumference (r = 0.115, p = 0.001), HDL cholesterol (r = −0.113, p = 0.002), and daily calcium intake (r = 0.697, p = 0.001). And, as the serum creatinine increased by 1, the risk of metabolic syndrome increased 16.5 times (OR: 16.452, 95% CI: 1.701–159.136, p < 0.05). Excessive phosphorus intake and high creatinine levels may increase the risk of metabolic syndrome in adolescents. Therefore, education is necessary to encourage adolescents to follow a balanced diet that contains essential minerals. In addition, it is suggested to expand the metabolic syndrome prevention education, which has been largely targeted towards adults.

PSII-13 Impact of maternal phosphorus intake on colostrum quality, calf growth, and calf immunoglobulin concentrations in primiparous beef cows

The objective of this experiment was to evaluate the effect of maternal phosphorus intake on growth and health of their calves. Treatments were 1) a free-choice mineral containing no supplemental P or 2) a free-choice mineral with 4% supplement phosphorus. Primiparous crossbred Angus beef cows (n = 36) were stratified by body weight and pregnancy status (bred by artificial insemination or natural service) then assigned to pasture groups (4 groups, 2/treatment, 9 heifers/group). These bred heifers had been receiving these same dietary treatments from 30 days after weaning until confirmation of pregnancy. Eighteen bred heifers from each treatment were selected randomly to continue into this experiment. At calving, colostrum and blood samples were collected from a subset of 12 heifers/treatment (6/group) and evaluated. Body weights and calf viability scores were obtained for all cattle. Data were analyzed using the MIXED (for continuous data) and GLIMMIX (for scoring data) procedures of SAS using group as the experimental unit. Cows grazed mixed grass pastures; monthly forage samples ranged from 0.28 to 0.36% P. There were no differences (P &gt; 0.10) for cow body weight during gestation, calf birth weight, calf viability scores at birth, or calf weight at an average age of 21 days. There were also no differences (P &gt; 0.10) in colostrum components (fat, protein, lactose, and IgG), or in the serum IgG or plasma mineral concentrations for both cows and calves 48 hours after parturition. All calves were sampled at approximately 21 days of age and there were no treatment differences (P &gt; 0.10) in serum IgG concentrations. There were no benefits to supplementing gestating heifers with phosphorus when they grazed pasture with a history of fertilization with livestock manure.

Circulating phosphorus level and risk of prostate cancer: a Mendelian randomization study

Background Recent observational studies have suggested that circulating phosphorus levels are positively associated with risk of prostate cancer. However, little is known about the causal direction of the association. Objective To explore the potential causal relationship between circulating phosphorus and risk of prostate cancer, we conducted a Mendelian randomization (MR) study. Design Summary statistics of prostate cancer were obtained from a meta-analysis of genome-wide association studies (GWAS) consisting of 79,148 cases and 61,106 controls. Single nucleotide polymorphisms (SNP) associated with serum phosphorus level were selected from a GWAS of 291,408 individuals from the UK Biobank. MR analysis was performed using the inverse-variance weighted (IVW) method, supplemented with simple-median, weighted-median, maximum likelihood-based, MR-Egger regression and MR-PRESSO test. We also performed a meta-analysis of observational studies to assess the associations of dietary phosphorus intake and serum phosphorus level with risk of prostate cancer. Results In the MR analysis, a total of 125 independent SNPs associated with serum phosphorus levels were used as instrumental variables. Genetically predicted serum phosphorus levels were associated with a 19% increased risk of prostate cancer (95% confidence interval (CI): 9%, 31%) per one SD increment of serum phosphorus by IVW (P = 1.82 × 10–4). Sensitivity analyses using alternative MR methods produced similar positive associations, and no evidence of pleiotropy was detected by MR-Egger regression (P = 0.422). For meta-analysis, eight studies for dietary phosphorus intake and four for serum phosphorus levels were included involving a total of 669,080 participants. Consistently, high dietary phosphorus intake and serum phosphorus levels were associated with an 8% (95% CI: 4%, 12%) and 7% (95% CI: 1%, 14%) increase in prostate cancer risk, respectively. Conclusions Our study suggested a potential causal relationship between circulating phosphorus and risk of prostate cancer. Further studies are warranted to elucidate the underlying mechanism of phosphorus in the development of prostate cancer.

Trends in Total, Added, and Natural Phosphorus Intake in Adult Americans, NHANES 1988–1994 to NHANES 2015–2016

Dietary phosphorus intake in the USA has been consistently greater than the Recommended Daily Allowance (RDA) with several studies reporting associations between intake and health risks as well as all-cause mortality within healthy subjects and patients with chronic kidney disease (CKD). The current study utilized a novel approach to calculate added phosphorus content in foods to determine sources (National Health and Nutrition Examination Survey, NHANES 2001–2016, n = 39,796) and trends in consumption (NHANES 1988–1994, 2001–2016, n = 55,744) of total, naturally occurring, and added phosphorus. Among adults (19+ years), the mean intake of total and natural phosphorus (mg/day) in 1988–1994 as compared with 2015–2016 increased (total: 1292 ± SE 11 vs. 1398 ± SE 17; natural: 1113 ± SE 10 vs. 1243 ± SE 16 mg/day); in contrast, added phosphorus intake decreased during this time (178 ± SE 2.9 vs. 155 ± SE 4.1 mg/day). Added phosphorus as a percent of total ranged from about 14.6% in 1988–1994 to about 11.6% in 2015–2016. The top five sources of total and naturally occurring phosphorus, representing approximately 20% of intake, were cheese, pizza, chicken (whole pieces), reduced-fat milk, and eggs/omelets. The top five sources of added phosphorus were cheese, soft drinks, cakes/pies, rolls/buns, and cookies/brownies, representing 45% of added phosphorus in the diet. Consumption of added phosphorus has decreased over the past few decades, possibly due to increased demand for foods with less additives/ingredients but may also be due to inaccurate phosphorus values in nutrition databases. Further studies are needed to validate the added phosphorus calculations utilized in this study and nutrition databases should consider providing added phosphorus content.

66 Strategies to Improve Phosphorus Utilization in Growing Pigs: Depletion-repletion Protocols

To optimize the use of dietary P by pigs, 5 feeding strategies were studied in a 3-phase feeding trial on 240 pigs (initial bodyweight (BW) of 31 kg): 1) C-C-C providing 100% of digestible phosphorus (Pdig, 4.3 g/kg STTD) and calcium (Ca, 9.7 g/kg) requirement to maximize bone mineralization, 2) L-L-L 60% of the Pdig and Ca requirements of C-C-C, 3) Phyt-Phyt-Phyt (phosphate-free, with phytase, 750, 686, 390 FTU/kg), providing 60% of Pdig and Ca requirements in phase 1, then 100%, 4) and 5) C in phases 1 and 3, and 60% of the need for Pdig in phase 2, associated with 65% of the requirements for Ca (N) or 80% (H), namely C-N-C and C-H-C. The BW and bone mineral content (BMC) were measured at the beginning and end of each phase. The BMC gain (gBMC), average daily gain (ADG) and average daily feed intake (ADFI) were calculated by phase. In phase 1, ADG was lower in the Phyt group than the C group (1.05 vs 1.10 kg/d, P &lt; 0.01) and the BMC of group C and gBMC were higher than those of the Phyt and B groups (P &lt; 0.05). In phase 2, C-C and Phyt-Phyt groups had similar BMC due to higher gBMC in the Phyt-Phyt (27.1 vs 18.4 g/d, P &lt; 0.01). At the end of phases 2 and 3, C-C-C, C-N-C and C-H-C groups had similar BMC. The Phyt and B groups showed an increased phosphorus-use efficiency during phases 1 and 2 (+20% vs C). Phosphorus retention was also higher in the C-N-C and C-H-C groups, during the depletion in phase 2 (+24% vs C, P&lt; 0.05). These results showed the potential of a depletion-repletion strategy including free phosphate diet to reduce phosphorus intake and excretion without affecting final growth performance and bone mineralization because of increased minerals utilization efficacies.

MO593CONTROLLING DIETARY PHOSPHORUS IN CHRONIC KIDNEY DISEASE STAGES 1 AND 2 DECREASES PROTEINURIA AND PREVENTS DECLINE IN RENAL FUNCTION

Background and Aims High phosphorus intake is known to cause renal and vascular calcification and renal tubular injury and albuminuria. Dietary phosphorus restriction is therapeutic for controlling disordered phosphorus homeostasis and for improving cardiovascular outcomes in CKD. However, early restriction of dietary phosphorus is not advocated Aim: To evaluate if early control of dietary phosphorus ameliorates proteinuria, prevents decline in glomerular filtration rate and prevents increase in FGF-23 Method One year longitudinal study on 79 CKD patients in stages 1 and 2. eGFR, serum creatinine , phosphorus, calcium, FGF-23, soluble α-Klotho iPTH FGF 23, blood pressure, were evaluated and compared with 35 controls. 3 days dietary intake was taken using standard methodology on first visit, 6 and 12 months. CKD patients were grouped based on dietary phosphorus intake: Group 1 (n 42): normal phosphorous intake (&lt;1000mg/day) and Group 2 (n=37; 17 in CKD 1; 20 CKD 2): high phosphorous intake (&gt;1000mg/d). Patients in Group 2 were educated on high and low phosphorus foods and counselled to avoid fresh and frozen and processed meat, eggs, nuts and seeds, chocolates, packaged food, phosphorus-containing food additives and counselled to adopt a plant-based diet, for low phosphorus availability/absorption diet with directed diet plan. Lentils and pulses, milk and milk products (hard cheese, ice-creams, custards, cottage cheese, pudding, yoghurt), bran and whole wheat cereals were restricted up to 1-2 servings a day Data were analysed using SPSS. Results At baseline there was no significant difference in the GFR (group1 85.00±18.64 ml/min vs group 2 82.53±16.30ml/min), serum creatinine between groups. In group2 ; GFR, sKlotho, serum phosphorus and FGF-23 correlated significantly with dietary phosphorus intake. In group 2, FGF-23, Serum phosphorus, dietary protein and phosphorus intake were significantly higher and sKlotho was significantly lower than group 1. There was significant difference in serum phosphorus (p 0.000), iPTH, (p 0.004), FGF23 (p0.000), Klotho (p0.000), urinary protein (p0.000), dietary protein (Group 1 37.57±3.40; Group 248.79±5.86 p 0.000) and phosphorus (Group 1868.96±69.99 mg/d and Group 2 1312.26±137.57 mg/d p 0.000) intake and dietary phosphorous to protein ratio (p 0.000) between groups 1 and 2.. After dietary intervention in group 2 GFR increased from 80.93±15.34 to 84.11±15.38 in six months and to 87.43±18.27 ml/min at 12 months p 0.012, and urinary protein declined to 22.01±3.39 mg/mL. FGF 23 declined from 60.67±6.26 to 58.00±7.07 to 53.29±9.48 pg/mL at 12 months. Urinary phosphorus excretion increased from 574.37±214.22 to 624.64±137.67 at 12 months. Dietary phosphorus protein to ratio reduced from 27.16±4.35 to24.75±4.34 p 0.000 at 12 months Conclusion CKD patients should be cautioned and counselled on their first visit on the impact of dietary phosphorus intake on the progression of CKD and development of CVD.

Dietary Phosphorus as a Marker of Mineral Metabolism and Progression of Diabetic Kidney Disease

Phosphorus is an essential nutrient that is critically important in the control of cell and tissue function and body homeostasis. Phosphorus excess may result in severe adverse medical consequences. The most apparent is an impact on cardiovascular (CV) disease, mainly through the ability of phosphate to change the phenotype of vascular smooth muscle cells and its contribution to pathologic vascular, valvular and other soft tissue calcification. Chronic kidney disease (CKD) is the most prevalent chronic disease manifesting with the persistent derangement of phosphate homeostasis. Diabetes and resulting diabetic kidney disease (DKD) remain the leading causes of CKD and end-stage kidney disease (ESRD) worldwide. Mineral and bone disorders of CKD (CKD-MBD), profound derangement of mineral metabolism, develop in the course of the disease and adversely impact on bone health and the CV system. In this review we aimed to discuss the data concerning CKD-MBD in patients with diabetes and to analyze the possible link between hyperphosphatemia, certain biomarkers of CKD-MBD and high dietary phosphate intake on prognosis in patients with diabetes and DKD. We also attempted to clarify if hyperphosphatemia and high phosphorus intake may impact the onset and progression of DKD. Careful analysis of the available literature brings us to the conclusion that, as for today, no clear recommendations based on the firm clinical data can be provided in terms of phosphorus intake aiming to prevent the incidence or progression of diabetic kidney disease.