Dietary Phosphorus Restriction Research Articles

Dietary Magnesium Intake and Proteinuria: Is There a Relationship?

The possible relationship between dietary magnesium status and proteinuria has been suggested by a number of previous studies. However, human studies on this association are limited. Therefore, the present study aimed to investigate the independent relationship between dietary magnesium intake and urinary protein excretion. The present study was a post hoc analysis of the previous randomized clinical trial that evaluated the effect of dietary phosphorus restriction on proteinuria. The baseline data of 90 participants with proteinuria and chronic kidney disease was used to measure the association between dietary magnesium intake and proteinuria. Participants were asked to record their 24-h food intake for three days a week in a questionnaire. Urinary protein to creatinine ratio (UPCR) in a random urine sample was measured to be a marker for proteinuria. Out of 90 patients included in the study, 47 were men and 43 were women. The mean ± standard deviation of age and body mass index were 59.05 ± 14.16 years and 29.02 ± 5.54 kg/m2, respectively. The patients' average daily dietary intake of energy and magnesium were 2183 kcal and 169.44 mg, respectively. A significant inverse correlation was found between the dietary intake of magnesium and UPCR (r = - 0.219, p = 0.042). This association remained significant even after adjusting for confounding variables (β = - 0.222, p = 0.028). The findings of the present study showed a significant inverse relationship between the magnesium intake and proteinuria. Although, the design of the current research was cross-sectional, it has provided a basis for conducting future longitudinal studies and trials to better elucidate such a relationship.

Urinary Phosphorus Excretion and Cardiovascular Outcomes in Patients with Pre-Dialysis Chronic Kidney Disease: The KNOW-CKD Study.

The relationship between 24-h urinary phosphorus excretion (24 h UPE) and cardiovascular disease in patients with pre-dialysis chronic kidney disease (CKD) has rarely been studied, despite the fact that the relationship between serum phosphorus level and the risk of a cardiovascular event is well established. A total of 1701 patients with pre-dialysis CKD were finally included for the analyses and were divided into tertiles by 24 h UPE (first tertile (T1, 349.557 (mean) ± 88.413 (standard deviation)), second tertile (T2, 557.530 ± 50.738), and third tertile (T3, 851.695 ± 171.593). The study outcome was a six-point major adverse cardiac event (MACE). The median follow-up duration was 7.992 years. Kaplan-Meier curve analysis visualized that the cumulative incidences of a six-point MACE (p = 0.029) significantly differed from 24 h UPE levels, as the incidence rate of the study outcomes was highest in T1 and lowest in T3. Cox proportional hazard models unveiled that, compared to T1, the risk of a six-point MACE was significantly decreased in T3 (adjusted hazard ratio (HR) 0.376, 95% confidence interval (CI) 0.207 to 0.683). The restricted cubic spline curve analysis visualized an inverted S-shaped association between 24 h UPE level and the risk of a six-point MACE, indicating a significantly increased risk of a six-point MACE in patients with a low 24 h UPE level. In conclusion, low 24 h UPE is associated with adverse cardiovascular outcomes in patients with CKD. Our finding emphasizes that low 24 h UPE should not be a reliable marker for dietary restriction of phosphorus that essentially leads to better outcomes in patients with CKD.

Acute High Dietary Phosphorus Following Low-Phosphorus Diet Acclimation Does Not Enhance Intestinal Fractional Phosphorus Absorption in Nephrectomized Male Rats.

Dietary phosphorus restriction and phosphorus binders are commonly prescribed for patients with chronic kidney disease (CKD). However, occurrences of non-adherence to these interventions are common. As low-phosphorus (LP) diets have been consistently experimentally shown in vitro to increase intestinal phosphorus absorption efficiency, a bout of non-adherence to diet or binders may cause an unintended consequence of enhanced intestinal phosphorus absorption. Thus, we aimed to determine the effect of a single bout of high-phosphorus (HP) intake after acclimation to a LP diet. Male Sprague Dawley rats with 5/6 nephrectomy (n=36) or sham operation (n=36) were block-randomized to 1 of 3 diets: LP (0.1% P w/w), HP (1.2%), or LP followed by acute HP (LPHP 0.1% then 1.2%). Phosphorus absorption tests were conducted using 33P radioisotope administrated by oral gavage or intravenously (iv). Although the overall two-way ANCOVA model for intestinal fractional phosphorus absorption was non-significant, exploratory comparisons showed intestinal fractional phosphorus absorption efficiency tended to be higher in rats in the LP compared with HP or LPHP groups. Rats in the HP or LPHP groups had higher plasma phosphorus compared with rats in the LP group, but the LPHP group was not different from the HP group. Gene expression of the major intestinal phosphate transporter, NaPi-2b, was lower in the jejunum of rats in the LPHP group compared with rats in the HP group but not different in the duodenum. These results demonstrate that an acute HP load after acclimation to a LP diet does not lead to enhanced intestinal fractional phosphorus absorption efficiency in 5/6 nephrectomized male rats. These data provide evidence against the notion that dietary phosphorus restriction or binder use adversely increases absorption efficiency after a single instance of dietary or binder non-adherence. However, other adverse consequences of fluctuating dietary phosphorus intake cannot be ruled out. © 2022 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

Effect of Dietary Phosphorous Restriction on Fibroblast Growth 2 Factor-23 and sKlotho Levels in Patients with Stages 1-2 Chronic Kidney Disease.

Hyperphosphatemia has emerged as an independent risk factor for cardiovascular disease (CVD) and excess mortality in chronic kidney disease (CKD). The study evaluates the effect of dietary phosphorus (Ph) restriction (DPhR) at an early stage as a therapeutic strategy for delaying CKD progression and preventing CVD. Methods: This was a one-year interventional study conducted on 79 stage 1 and 2 CKD patients. The dietary phosphorus intake (DPhI), fibroblast growth factor-23 (FGF-23), sKlotho and serum phosphorous (SP) levels were analyzed. Patients were categorized into two groups based on their DPhI, recommended DPhI (RPhI) with <1000 mg/day of dietary phosphorous (dietary counselling) and high DPhI (HPhI) with >1000 mg/day (dietary intervention). For comparisons of differences between the two groups, independent t-test; for correlation analysis, Pearson correlation; for identifying the significant associated risk factors for CKD, binary logistic regression analysis and for comparing the means across the three visits, repeated measures ANOVA were used for statistical analysis. Results: The mean age and glomerular filtration rate (GFR) of CKD patients were 38 ± 12 years and 82.95 ± 16.93 mL/min/1.73 m2. FGF-23, SP, dietary protein and DPhI were significantly higher and sKlotho was significantly lower in HPhI group than RPhI group. In HPhI group; GFR, sKlotho, SP and FGF-23 correlated significantly with DPhI. Risk factors with a statistical bearing on the progression of CKD were animal-based diet, family history of CKD and hypertension. In HPhI group; GFR, DPhI, SP and FGF-23 levels significantly improved within the intervention period whereas a significant increase in sKlotho levels was observed in both the groups. Conclusion: Restricting DPhI emerged as a favorable therapeutic strategy for CKD patients for improving renal function and controlling hyperphosphatemia. The results of the present study may serve as the basis for future interventional studies with dietary phosphate restriction in the initial stages of CKD that would preserve renal function. Highlights: Early restriction of dietary phosphorus prevents decline in eGFR, elevation in FGF23 and increases Klotho levels.

The Interplay between Dietary Phosphorous, Protein Intake, and Mortality in a Prospective Hemodialysis Cohort.

(1) Background: Current dietary recommendations for dialysis patients suggest that high phosphorus diets may be associated with adverse outcomes such as hyperphosphatemia and death. However, there has been concern that excess dietary phosphorus restriction may occur at the expense of adequate dietary protein intake in this population. We hypothesized that higher dietary phosphorus intake is associated with higher mortality risk among a diverse cohort of hemodialysis patients. (2) Methods: Among 415 patients from the multi-center prospective Malnutrition, Diet, and Racial Disparities in Kidney Disease Study, we examined the associations of absolute dietary phosphorus intake (mg/day), ascertained by food frequency questionnaires, with all-cause mortality using multivariable Cox models. In the secondary analyses, we also examined the relationship between dietary phosphorus scaled to 1000 kcal of energy intake (mg/kcal) and dietary phosphorus-to-protein ratio (mg/g) with survival. (3) Results: In expanded case-mix + laboratory + nutrition adjusted analyses, the lowest tertile of dietary phosphorus intake was associated with higher mortality risk (ref: highest tertile): adjusted HR (aHR) (95% CI) 3.33 (1.75–6.33). In the analyses of dietary phosphorus scaled to 1000 kcal of energy intake, the lowest tertile of intake was associated with higher mortality risk compared to the highest tertile: aHR (95% CI) 1.74 (1.08, 2.80). Similarly, in analyses examining the association between dietary phosphorus-to-protein ratio, the lowest tertile of intake was associated with higher mortality risk compared to the highest tertile: aHR (95% CI) 1.67 (1.02–2.74). (4) Conclusions: A lower intake of dietary phosphorus was associated with higher mortality risk in a prospective hemodialysis cohort. Further studies are needed to clarify the relationship between specific sources of dietary phosphorus intake and mortality in this population.

Currently Available Handouts for Low Phosphorus Diets in Chronic Kidney Disease Continue to Restrict Plant Proteins and Minimally Processed Dairy Products

The 2020 Kidney Disease Outcome Quality Initiative guidelines recommend adjusting phosphorus intake to achieve and maintain normal serum phosphorus levels for adults living with chronic kidney disease. These guidelines also recommend considering the dietary source of phosphorus as different sources have different bioavailability; however, phosphorus food lists are not provided. Therefore, the aim of this study is to investigate the current teaching materials in Canada regarding low phosphorus diet. Using a geographical approach, websites from each province and territories' government, health, and renal programs (where applicable) were reviewed for resources on dietary phosphorus restriction in chronic kidney disease. All publicly available handouts/booklets/printable webpages were obtained and reviewed for recommendations on how to implement a low phosphorus diet. Sixty-one resources in total met inclusion criteria (52 handouts from health agencies in 6 provinces and 9 handouts from the Kidney Foundation of Canada). Items with minimal nutrition value, such as cola, beer and cocoa, chocolate, and baking powder, were the most commonly restricted with 84% (51/61) resources making this recommendation. Plant proteins and minimally processed dairy were restricted in 80% (49/61) of resources. Processed animal meat was recommended to be restricted in 70% (43/61) of resources and whole grains in 65% (40/61). Sixty-three percent of the handouts (39/61) discuss avoiding phosphorus additives. Many resources restrict items with minimal nutrition value to lower phosphorus intake; however, plant foods, including plant proteins and whole grains, continue to be restricted in the majority of resources, despite having lower bioavailability. The 2020 Kidney Disease Outcome Quality Initiative guidelines recommend considering bioavailability of phosphorus source when implementing low phosphorus diets; current handouts in Canada would likely benefit from review.

290 Dietary Phosphorus Restriction in Early Stages of Chronic Kidney Disease Improves Renal Function, and Controls CKD-MBD and Cardiovascular Risk Factors

290 Dietary Phosphorus Restriction in Early Stages of Chronic Kidney Disease Improves Renal Function, and Controls CKD-MBD and Cardiovascular Risk Factors

Effect of dietary calcium and phosphorus restriction during grower period on growth performance, carcass traits, blood and bone parameters and broiler chickens adaptation in finisher period

Effect of dietary calcium and phosphorus restriction during grower period on growth performance, carcass traits, blood and bone parameters and broiler chickens adaptation in finisher period

Phosphorus Restriction in Brooding Stage Has Continuous Effects on Growth Performance and Early Laying Performance of Layers.

Simple SummaryPhosphorus plays a critical role in bone and eggshell formation. Dietary phosphorus oversupply depletes non-renewable natural resources and causes environmental concerns in animal husbandry. This study evaluated the effects of phosphorus restriction in the brooding stage and subsequent recovery on growth performance, tibia development and early laying performance of layers. Phosphorus restriction decreases growth performance and bone characters in the brooding stage, and the adverse effects on body weight and early laying performance do not disappear after phosphorus supplementation. These findings give a foundation and new perspective on low phosphorus feeding strategies in the production of layers.This study evaluated the effects of phosphorus restriction in the brooding stage and subsequent recovery on growth performance, tibia development and early laying performance of layers. 360 one-day-old hens were randomly divided into 4 groups with 6 replicates and 15 chicks per replicate. Chicks were fed diets containing 0.13% (L), 0.29% (M), 0.45% (N), 0.59% (H) non-phytate phosphorus (nPP) from 1 to 8 weeks of age. From 9 to 20 weeks of age, the L and N group were divided into two groups fed normal level phosphorus (n, 0.39% nPP) and high-level phosphorus (h, 0.45% nPP) separately, then all the birds were fed a normal diet (0.39% nPP) from 21 to 26 weeks of age. Four treatments were tested: Ln, Lh, Nn, and Nh. The lower body weight, average daily feed intake, tibia length and daily tibial increment were observed in the L group (p < 0.05) and the ratio of feed to gain was significantly increased in the L group at 8 weeks of age (p < 0.05). In addition, the fresh and degreased tibia weight, bone ash, Ca content in the tibia and P content in the ash and tibia were significantly decreased in the L group at 8 weeks of age (p < 0.05). After compensatory processes, there was no significant difference in tibia characters; however, body weight in the Ln group was significantly lower than in the Nn group (p < 0.05) and was significantly lower in the Lh group than the Nn group (p < 0.01) and Nh group (p < 0.05). In addition, the laying rate and average daily egg mass in the Lh group were lower than Nn and Nh (p < 0.05). In conclusion, severe dietary phosphorus restriction impaired growth performance and bone mineralization in the brooding stage. Subsequent phosphorus supplementation could not alleviate this adverse effect on body weight, which continued to affect egg production. These findings give a foundation and new perspective on a low phosphorus feeding strategy in layer production.

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

Abstract 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 (&amp;lt;1000mg/day) and Group 2 (n=37; 17 in CKD 1; 20 CKD 2): high phosphorous intake (&amp;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.

The Effect of Dietary Phosphorus Restriction on Urine Protein Excretion in Patients With Proteinuria: A Randomized Controlled Trial

The present study was designed to determine the effect of dietary phosphorus restriction, independent of protein intake, on the urinary protein excretion in patients with proteinuria. Seventy-one patients with proteinuria were enrolled in a parallel randomized controlled trial study. The patients were randomly allocated to receive either a recommended phosphorus-restricted diet (n=36) or a recommended control diet (n=35), for 8weeks. A diet was designed and recommended to participants in a way that both trial groups would receive the same amount of energy and protein and the only significant difference between them was the amount of phosphorus intake. The study outcomes included the changes in spot urine protein-to-creatinine ratio, the changes in serum and urine levels of phosphorus, as well as the changes in estimated glomerular filtration rate (eGFR). The mean±standard deviation of age, body mass index, and eGFR of the participants were 59±14years, 29±5.5kg/m2, and 56.1±21.7mL/min/1.73m2, respectively. The amount of phosphorus intake decreased significantly in the phosphorus-restricted group compared to the control one (-709 vs. -369mg/day; P<.001). This decrease is accompanied by a significant reduction in urine protein-to-creatinine ratio in the phosphorus-restricted group; however, this change did not reach a significant level when compared to the control one (the mean change: -75.78 vs. -55.25mg/g; P=.539). Limiting the phosphorus intake did not change its serum and urine values as well as eGFR at the end of the trial. Although adherence to a phosphorus-restricted diet by patients with proteinuria led to a significant decrease in urinary protein excretion, this change was not significantly different from that of the control diet. Further studies with larger sample sizes and different designs will reveal more evidence for a link between phosphorus intake and proteinuria.

Full-Scale Clinical Data and Reshaped Intestinal Microbiome on a Short-Term Low-Phosphorus Diet among Healthy Adults

During the past few decades, phosphorus intake has dramatically increased along with higher protein intake and overuse of inorganic phosphate additives worldwide. The detrimental effects of overconsumption of phosphorus are well recognized for patients with chronic kidney disease (CKD), and dietary phosphorus restriction was recommended for these patients. However, the effects of dietary phosphorus restriction in healthy people have not been fully studied. In this open-label crossover study, healthy adult men (n=12) consumed normal phosphorus diet (NPD, 1,500mg/d) for fivedays. After a 10-day washout period, healthy adults took low phosphorus diet (LPD, 500mg/d) for another fivedays. On the fifth day of each intervention, blood, urine and saliva samples were collected at ten time points, and fecal specimens were collected for bacterial taxa identification. We found that 24-h mean levels of serum phosphate (Pi), urinary Pi, serum parathyroid hormone and fibroblast growth factor 23 decreased, while serum calcium (Ca) and 1,25-dihydroxy vitamin D increased significantly under LPD compared with those under NPD. Dietary phosphorus intake did not change salivary Pi, urinary Ca, salivary Ca and magnesium (Mg) metabolism. Compared with NPD, LPD increased the relative abundance of beneficial microbes including Bacteroidetes, Ruminococcaceae and Lachnospiraceae, indicating that multiple bacterial metabolic pathways have been shifted. Full-scale data of dietary phosphorus restriction on Pi, Ca and Mg metabolism in healthy male adults are provided. More importantly, for the first time, dietary phosphorus restriction was found to reshape the intestinal microbiome, which provides information for benefits of dietary phosphorus restriction in healthy people, and potential clues for treating patients with CKD.

Urinary Phosphate Excretion and Microvascular Function in a Population-Based Cohort

Urinary Phosphate Excretion and Microvascular Function in a Population-Based Cohort

Dietary Phosphorus Restriction Improves Renal Function, Blood Pressure, FGF-23, and Klotho Levels in CKD Stages 1 and 2

Dietary Phosphorus Restriction Improves Renal Function, Blood Pressure, FGF-23, and Klotho Levels in CKD Stages 1 and 2

Phosphatemic Index Is a Novel Evaluation Tool for Dietary Phosphorus Load: A Whole-Foods Approach

Dietary phosphorus (P) restriction is crucial to treat hyperphosphatemia and reduce cardiovascular disease risk and mortality in patients with chronic kidney disease (CKD) and the wider population. Various methods for dietary P restriction exist, but the bioavailability of P in food should also be considered when making appropriate food choices to maintain patients' quality of life. Here, we propose the "Phosphatemic Index" (PI) as a novel tool for evaluating dietary P load based on P bioavailability; we also evaluated the effect of continuous intake of different PI foods in mixed meals on serum intact fibroblast growth factor 23 concentration. A 2-stage crossover study was conducted: Study 1: 20 healthy participants consumed 10 different foods containing 200mg of P, and the PI was calculated from the area under the curve of a time versus serum P concentration curve; Study 2: 10 healthy participants consumed 4 different test meals (low, medium, or high PI meals or a control) over a 5-day period. Study 1 showed milk and dairy products had high PI values, pork and ham had medium PI values, and soy and tofu had low PI values. In Study 2, ingestion of high PI test meals showed higher fasting serum intact fibroblast growth factor 23 levels and lower serum 1,25-dihydroxyvitamin D levels compared with ingestion of low PI test meals. These findings suggest that the PI can usefully evaluate the dietary P load of various foods and may help to make appropriate food choices for dietary P restriction in CKD patients.

Translation of Nutrient Level Recommendations to Control Serum Phosphate Into Food-Based Advice

The control of hyperphosphatemia is key to the management of chronic kidney disease mineral and bone disorder. Dietary restriction of phosphorus is essential to control hyperphosphatemia. Guidelines for chronic kidney disease and end-stage kidney disease generally provide high-level guidance on whether a nutrient should be restricted e.g, restrict dietary phosphorus. Dietitians translate such guidance into nutrient-based strategies and finally into food-based practical dietary advice for patients to follow. The practical aspects of dietary advice are not well described in the literature, neither are the challenges of concurrently altering 1 nutrient e.g., phosphorus while continuing to restrict others e.g., potassium, while maintaining overall nutritional adequacy and quality of life. In this article, we describe how we translated updated nutrient level recommendations into practical dietary advice to be delivered at the bedside.

Novel Approaches for Dietary Phosphorus Management in Chronic Kidney Disease

&lt;p&gt;Conventional approaches to alleviating hyperphosphatemia in patients with Chronic Kidney Disease (CKD) include dietary phosphorus restriction and use of phosphate binders. These approaches are, however not enough to control hyperphosphatemia and hence the need for novel nutritional approaches arises. Dietary phosphorus, protein and phytate values of some common food ingredients were obtained. Phosphates to protein ratio and net phosphorus absorption from the gut were reported on the basis of the phytate content of these ingredients. Among some common Indian food ingredients, phosphate to protein ratio was high in cereals, millets and dairy products. However due to presence of high amount of phytate, the net absorption of phosphate was lower from plant based sources of phosphorus as compared to animal based sources. It can be concluded that phosphorus to protein ratio is a metric which helps to ensure dietary phosphorus restriction with sufficient intake of proteins. Tables providing phosphorus to protein ratio along with phytate and per cent absorption may prove to be beneficial in achieving desired target levels of phosphorus for renal dieticians in case of CKD patients with hyperphosphatemia.&lt;/p&gt;

Restriction of dietary non-phytate phosphorus on growth performance and expression of intestinal phosphate cotransporter genes in broilers

Effects of dietary non-phytate phosphorus (nPP) restriction on growth and duodenal type IIb sodium-dependent phosphate cotransporter (NaPi-IIb) genes were observed. A total of 432 one-day old Cobb500 male broiler chickens in 36 cage pens were divided into 6 groups with each group containing 6 pens. Each group was treated with one of the diets containing 0.33, 0.37, 0.41, 0.45, 0.49, and 0.53% of nPP up to 14 D. During 15 to 31 D, birds were treated with one of the diets containing 0.23, 0.27, 0.31, 0.35, 0.39, and 0.43% of nPP. Level of Ca was kept the same across all treatments. Dietary nPP level influenced (P < 0.001) weight gain and feed intake in both growth phases, whereas effect on feed per gain ratio was seen only in the second phase. Toe ash, tibia ash, and tibia breaking strength responded to treatments (P < 0.01) at 14 D. Only tibia ash content was significantly improved (P < 0.001) at 31 D. Growth and bone parameters linearly improved with an increase in dietary nPP content (P < 0.05). Above dietary nPP 0.41% and 0.31% for first phase and second phase, respectively, no significant improvement was seen. Duodenal NaPi-IIb mRNA overexpressed with a decrease in dietary nPP in both phases (P < 0.05). Relative expression of NaPi-IIb in lowest nPP group were 2.2 folds higher in the first phase and 3.6 folds higher in the second phase compared to respective highest nPP groups of each phase. No significant change in NaPi-IIb expression was seen above 0.37% of dietary nPP for 14 D and 0.31% of dietary nPP for 31 D. Dietary requirements of nPP 0.41% for 0 to 14 D and 0.31% for 15 to 31 D were adequate for optimal growth and bone parameters. This study fills the gap in understanding of intestinal NaPi-IIb expression in response to dietary nPP restriction in broilers older than 21 D of age.

Chronic Kidney Disease: Treatment of Comorbidities I: (Nutrition, Growth, Neurocognitive Function, and Mineral Bone Disease).

This review discusses the complications of nutrition, growth, neurocognitive function and mineral and bone disorder in pediatric chronic kidney disease. We discuss the most recent evidence-based methods for evaluation and prevention of these complications in addition to treatment strategies to address the complications and mitigate adverse effects. Frequent nutritional assessment is important, particularly for infants and young children. Due to anorexia, oral aversion and dietary restrictions, weight gain may be difficult to achieve. Adequate nutrition is important for growth. Children with CKD tend to be short, which can impact quality of life and social achievements. Once nutrition is optimized, growth hormone is an effective, but underutilized strategy to improving terminal height. Mineral and bone disorder is a difficult but common complication of CKD which may present with and be driven by abnormalities in calcium, phosphorus and parathyroid hormone levels. Treatment strategies include dietary phosphorus restriction, phosphorus binders, and inactive vitamin D and active vitamin D sterols. Effective treatment may reduce the risk for bone deformities, growth abnormalities, fractures, cardiovascular disease and mortality. Children with CKD also suffer from cognitive difficulties. Control of anemia, aggressive childhood nutrition, and decreased exposure to heavy metals (via dialysate and dietary binding agents) has provided substantial improvement to the more profound neurocognitive sequelae observed prior to the 1990s. Current prevention of cognitive sequelae may best be directed at improved blood pressure control and augmented school support. Pediatric CKD has systemic ramifications and can impact all aspects of normal development, including nutrition, growth, bone and mineral metabolism and neurocognitive function. Regular evaluation for disease complications and prompt treatment can reduce the untoward effects of CKD thereby improving the quality and duration of life.

Short-term effect of the New Nordic Renal Diet on phosphorus homoeostasis in chronic kidney disease Stages 3 and 4.

The New Nordic Diet is a food concept favouring organically produced food items, fruits, vegetables, whole grains and fish. We investigated the short-term effects of a modified phosphorus-reduced New Nordic Renal Diet (NNRD) in chronic kidney disease (CKD) patients on important parameters of phosphorus homoeostasis. The NNRD contained a total of 850 mg phosphorus/day. A total of 18 patients, CKD Stages 3 and 4 were studied in a randomized crossover trial comparing a 1-week control period of the habitual diet with a 1-week period of the NNRD. Data were obtained at baseline and during 1 week of dietary intervention (habitual diet versus NNRD) by collecting fasting blood samples and 24-h urine collections. The primary outcome was the difference in the change in 24-h urine phosphorus excretion from baseline to Day 7 between the NNRD and habitual diet periods. Secondary outcomes were changes in the fractional excretion of phosphorus, fibroblast growth factor 23 (FGF23) and plasma phosphate. As compared with the habitual diet, 24-h urine phosphorus excretion was reduced in the NNRD by 313 mg/day (P < 0.001). The mean baseline phosphorus was 875 ± 346 mg/day and was decreased by 400 ± 256 mg/day in the NNRD and 87 ± 266 mg/day in the habitual diet. The 24-h urine fractional excretion of phosphorus decreased by 11% (P < 0.001) and FGF23 decreased by 30 pg/mL (P = 0.03) with the NNRD compared with the habitual diet. Plasma phosphate did not change. This study demonstrates that dietary phosphorus restriction in the context of the NNRD is feasible and has positive effects on phosphorus homeostasis in CKD patients.