A New Disease Concept in the Age of Processed Foods-Phosphorus-Burden Disease; including CKD-MBD Concrete Analysis and the Way to Solution.

In 2012, the Japanese Society for Dialysis Therapy (JSDT) established the order of correction of P, corrected Ca (cCa), and whole PTH (w-PTH) in the treatment of Chronic Kidney Disease-Metabolic Bone Disorder (CKD-MBD) as P-first. However, there is no report that analyzes whether this rule is in line with reality and what the adequate rate of P is. Therefore, we analyzed the test values of our 48 patients during the year of 2019 and examined the validity of the results. The results showed that the adequate range rates were 70.8% for P, 100% for cCa, and 89.6% for w-PTH. This result is better than the JSDT Web-based Analysis of Dialysis Data Archives (WADDA) P adequacy rate of 66.2%. Although the guideline is P-first, it is often the case that we cannot reach the adequate level; therefore, healthcare professionals and patients often blame each other. We believe that this is due to the mismatch between the modern era of processed foods covered with P additives and treatment methods (P intake restriction and P-binders). The development of processed foods with P additives has brought light and darkness to mankind. The light side is freedom from starvation, and the dark side is a new condition caused by P burden: P burden disease including CKD-MBD.

Phosphate, Microbiota and CKD.

Phosphate is a key uremic toxin associated with adverse outcomes. As chronic kidney disease (CKD) progresses, the kidney capacity to excrete excess dietary phosphate decreases, triggering compensatory endocrine responses that drive CKD-mineral and bone disorder (CKD-MBD). Eventually, hyperphosphatemia develops, and low phosphate diet and phosphate binders are prescribed. Recent data have identified a potential role of the gut microbiota in mineral bone disorders. Thus, parathyroid hormone (PTH) only caused bone loss in mice whose microbiota was enriched in the Th17 cell-inducing taxa segmented filamentous bacteria. Furthermore, the microbiota was required for PTH to stimulate bone formation and increase bone mass, and this was dependent on bacterial production of the short-chain fatty acid butyrate. We review current knowledge on the relationship between phosphate, microbiota and CKD-MBD. Topics include microbial bioactive compounds of special interest in CKD, the impact of dietary phosphate and phosphate binders on the gut microbiota, the modulation of CKD-MBD by the microbiota and the potential therapeutic use of microbiota to treat CKD-MBD through the clinical translation of concepts from other fields of science such as the optimization of phosphorus utilization and the use of phosphate-accumulating organisms.

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

OBJECTIVE: 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. DESIGN AND METHODS: A 2-stage crossover study was conducted: Study 1: 20 healthy participants consumed 10 different foods containing 200 mg 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. RESULTS: 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. CONCLUSION: 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.

Does a rise in plasma erythropoietin after high-altitude exposure affect FGF23 in healthy volunteers on a normal or low-phosphorus diet?

BACKGROUND AND AIMS: Data of experimental rodent models suggest that hypoxia with subsequent increase in erythropoietin stimulates the expression of the phosphaturic hormone fibroblast growth factor 23 (FGF23). METHODS AND RESULTS: To translate the findings of animal studies into human physiology, herein we exposed eight healthy volunteers to high altitude (2656 m above sea level) for four days. The volunteers were randomized on a low-phosphorous diet (n = 4) or a normal phosphorus diet (n = 4). Although high-altitude exposure caused a significant increase in plasma erythropoietin (EPO) (before high-altitude exposure: low phosphorus: median EPO 6.6 mIU/ml [interquartile range (IQR) 6.0; 8.2], normal phosphorus: median EPO 9.0 mIU/ml [IQR 7.9; 11.5]; at day 2: low phosphorus: median EPO 21.3 mIU/ml [IQR 19.5; 23.8], normal phosphorus: median EPO 19.4 mIU/ml [IQR 18.0; 20.8]), there was no consistent increase in plasma c-terminal FGF23 or plasma intact FGF23. We observed only a single, intermittent peak in c-terminal FGF23 levels after 5 h of maximal aerobic exercise. CONCLUSION: These data do not support a substantial effect of moderate hypoxia alone on the expression of FGF23, but they suggest that combined exercise and high-altitude exposure may temporarily induce FGF23 expression.

The impact of a nutritional intervention based on egg white for phosphorus control in hemodialyis patients.

BACKGROUND AND AIMS: Here we describe a dietary intervention for hyperphosphatemia in dialysis patients based on the partial replacement of meat and fish, which are one of the main sources of alimentary phosphorous, with egg white, a virtually phosphorous-free protein source. This intervention aims to reduce phosphorous intake without causing protein wasting. PATIENTS AND METHODS: As many as 23 hyperphosphatemic patients (15 male and 8 female, mean age 53.0 ± 10.0 years) on chronic standard 4 h, three times weekly, bicarbonate hemodialysis were enrolled in this open-label, randomized controlled trial. Patients in the intervention group were instructed to replace fish or meat with egg white in three meals a week for three months whereas diet was unchanged in the control group. RESULTS: Serum phosphate concentrations were significantly lower in the intervention group than in controls after three (4.9 ± 1.0 vs 6.6 ± 0.8; p < 0.001) but not after one month of treatment. Phosphate concentrations decreased more from baseline in the intervention than in the control group both after one (-1,2 ± 1,1 vs 0,5 ± 1,1; p = 0.004) and after three (-1,7 ± 1,1 vs -0,6 ± 1,1; p < 0.001) months of follow-up. No change either in body weight or in body composition assessed with bioelectrical impedance analysis or in serum albumin concentration was observed in either group. CONCLUSION: The partial replacement of meat and fish with egg white induces a significant decrease in serum phosphate without causing protein malnutrition and could represent a useful instrument to control serum phosphate levels in hemodialysis patients. CLINICALTRIALS. GOV IDENTIFIER: NCT03236701.

Not all forms of dietary phosphorus are equal: an evaluation of postprandial phosphorus concentrations in the plasma of the cat.

Phosphorus is present in diets as naturally occurring P from raw materials or added as an inorganic salt. However, little is known about postprandial kinetics of P absorption in cats. Here, we describe several studies quantifying postprandial kinetics following the ingestion of diets of varying composition. Briefly, cats were fed a meal consisting of 50 % of their metabolic energy requirement in a randomised crossover design. A pre-meal baseline blood sample was taken via cephalic catheter and repeated measurements taken regularly up to 6 h post-meal to assess the whole blood ionised Ca, plasma P and parathyroid hormone concentrations. A diet containing 4·8 g total P/4184 kJ (1000 kcal), 3·5 g P from sodium dihydrogen phosphate (NaH2PO4)/4184 kJ (1000 kcal) and Ca:P 0·6 caused a marked increase in plasma P from baseline to a peak of 1·976 (95% CI 1·724, 2·266) mmol/l (P <0·001), whereas a diet containing 3·38 g total P/4184 kJ (1000 kcal), no added inorganic P and Ca:P 1·55 resulted in a postprandial decrease in plasma P (P = 0·008). Subsequent data indicate that added inorganic P salts in the diet above 0·5 g P/4184 kJ (1000 kcal) cause an increase in plasma P in cats, while diets below this do not. The data presented here demonstrate that sources of added inorganic P salts cause a temporary postprandial increase in plasma P in a dose-dependent manner, prolonged in diets with Ca:P <1·0. Dietary P derived from natural food ingredients (e.g. meat or vegetable matter) does not appear to have any effect on postprandial plasma P.

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.

Prevention and treatment of hyperphosphatemia in chronic kidney disease.

Hyperphosphatemia has consistently been shown to be associated with dismal outcome in a wide variety of populations, particularly in chronic kidney disease (CKD). Compelling evidence from basic and animal studies elucidated a range of mechanisms by which phosphate may exert its pathological effects and motivated interventions to treat hyperphosphatemia. These interventions consisted of dietary modifications and phosphate binders. However, the beneficial effects of these treatment methods on hard clinical outcomes have not been convincingly demonstrated in prospective clinical trials. In addition, exposure to high amounts of dietary phosphate may exert untoward actions even in the absence of overt hyperphosphatemia. Based on this concept, it has been proposed that the same interventions used in CKD patients with normal phosphate concentrations be used in the presence of hyperphosphatemia to prevent rise of phosphate concentration and as an early intervention for cardiovascular risk. This review describes conceptual models of phosphate toxicity, summarizes the evidence base for treatment and prevention of hyperphosphatemia, and identifies important knowledge gaps in the field.

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.

Impact of nutritional index on the association between phosphorus concentrations and mortality in haemodialysis patients: a cohort study from dialysis outcomes and practice pattern study in Japan.

OBJECTIVES: While maintenance of both phosphorus concentration and nutritional status is a major concern in managing haemodialysis patients, the interaction between these parameters is not well understood. The aim of this study was to assess whether or not nutritional index influences the association between phosphorus concentration and all-cause mortality. DESIGN: A cohort study. SETTING: The Dialysis Outcomes and Practice Pattern Study, which included 99 representative dialysis facilities in Japan between 1997 and 2010. PARTICIPANTS: A total of 6230 adult haemodialysis patients who had spent at least 6 months on haemodialysis. MAIN PREDICTORS: Six categories based on time-averaged factors of the geriatric nutritional risk index (GNRI; the lowest two and highest tertiles) and phosphorus concentration (<3.5, 3.5 to <6 and ≥6 mg/dL). PRIMARY OUTCOME MEASURE: All-cause mortality rate. ANALYSIS: Time-dependent Cox regression adjusting for potential confounders. RESULTS: During the follow-up period (12 294 person-years), we noted 561 deaths (4.6 per 100 person-years), and both high phosphorus concentrations and low-middle GNRI were separately associated with all-cause mortality. The harmful effect of high phosphorus concentrations on all-cause mortality was stronger in patients with high GNRI than in those with low-middle GNRI. On the other hand, the harmful effect of low phosphorus concentrations was stronger in those with low-middle GNRI than in those with high GNRI. Relative excess risk due to interaction (RERI) between high phosphorus concentrations and low-middle GNRI was -0.57, indicating an antagonistic interaction. We also observed a significant statistical multiplicative interaction between phosphorus concentrations and GNRI (p=0.05 by likelihood ratio test). CONCLUSIONS: The association between time-averaged serum phosphorus concentration and all-cause mortality differs across the nutritional index. Accordingly, nutritional index should be considered when the impact of phosphorus concentration on mortality in haemodialysis patients is evaluated.

Effects of serum phosphorus on vascular calcification in a healthy, adult population: A systematic review.

Cardiovascular disease has been associated with elevated serum phosphorus levels, which have been associated with cardiovascular mortality. This is commonly seen in the chronic kidney disease (CKD) population where studies have shown that high phosphorus levels cause coronary artery calcification. Although studies have independently associated vascular stiffness and serum phosphorus in those with and without CKD, there are fewer data in individuals without CKD. Therefore, the aim of this systematic review was to analyze whether serum phosphorus levels are associated with cardiovascular calcification in healthy individuals. A systematic review of the literature that was conducted revealed 10 articles, all cross-sectional studies, that met eligibility criteria. These criteria were peer-reviewed studies on a healthy, adult population written in the English language. Studies lacking data on serum phosphorus and measured to assess its association with vascular calcification were excluded. Studies on subjects with CKD, other chronic diseases, or on children were also excluded. Of the 10 studies located, 8 indicated an association between serum phosphorus and vascular calcification. One study did not indicate an association. One study indicated a statistically significant association between serum phosphorus and vascular calcification prevalence, but not incidence. Studies were limited since no randomized controlled trials were available. This systematic review generates gaps in research. Due to considerable amounts of phosphorus additives in the food supply, there may be a connection to dietary phosphorus and vascular calcification. Additionally, phosphorus binders may assist in the prevention of vascular calcification but have not been studied in a healthy population. Further study on both dietary phosphorus restriction and phosphorus binders is needed. While 8 out of 10 cross-sectional studies found an association in this systematic review, the topic of vascular calcification and serum phosphorus needs further study if a cause and effect relationship is to be detected.

Effect of stage-based education provided by dedicated dietitians on hyperphosphataemic haemodialysis patients: results from the Nutrition Education for Management of Osteodystrophy randomised controlled trial.

BACKGROUND: The Nutrition Education for Management of Osteodystrophy trial showed that stage-based nutrition education by dedicated dietitians surpasses existing practices in Lebanon with respect to lowering serum phosphorus among general haemodialysis patients. The present study explores the effect of nutrition education specifically on hyperphosphataemic patients from this trial. METHODS: Hyperphosphataemic haemodialysis patients were allocated to a dedicated dietitian (DD), a trained hospital dietitian (THD) and existing practice (EP) protocols. From time-point (t)-0 until t-1 (6 months), the DD group (n = 47) received 15 min of biweekly nutrition education by dedicated dietitians trained on renal nutrition; the THD group (n = 89) received the usual care from trained hospital dietitians; and the EP group (n = 42) received the usual care from untrained hospital dietitians. Patients were followed-up from t-1 until t-2 (6 months). Analyses used two-way repeated measures analysis of variance and Cohen's effect sizes (d). RESULTS: At t-1, phosphataemia significantly decreased in all groups (DD:-0.27 mmol L-1 ; EP:-0.15 mmol L-1 ; THD:-0.12 mmol L-1 ; P < 0.05); the DD protocol had the greatest effect relative to EP (d = -0.35) and THD (d = -0.50). Only the DD group showed more readiness to adhere to a low phosphorus diet at t-1; although, at t-2, this regressed to baseline levels. The malnutrition inflammation score remained stable only in the DD group, whereas the EP and THD groups exhibited a significant increase (DD: 6.74, 6.97 and 7.91; EP: 5.82, 8.69 and 8.13; THD: 5.33, 7.92 and 9.42, at t-0, t-1 and t-2, respectively). CONCLUSIONS: The results of the present study suggest that the DD protocol decreases serum phosphorus compared to EP and THD, at the same time as maintaining the nutritional status of hyperphosphataemic haemodialysis patients. Assessing the cost-effectiveness of the DD protocol is recommended.

Modified Nutritional Recommendations to Improve Dietary Patterns and Outcomes in Hemodialysis Patients.

The renal diet has traditionally been regarded as one of the most complex medical nutrition therapies to teach, understand, and implement. Specifically, patients are instructed to limit fruits, vegetables, nuts, legumes, dairy, and whole grains because of both phosphorus and potassium concerns. Furthermore, hemodialysis patients are often encouraged to decrease fluid intake to control interdialytic weight gain. These restrictions can result in frustration, lack of autonomy, and the perception that there is nothing left to eat. It is possible that the traditional renal diet may be liberalized, with a focus on whole foods low in sodium and phosphorus additives, to afford patients greater choices and ultimately improved outcomes. Therefore, the objective of this review is to concisely assess the evidence in support of a renal diet focused primarily on reducing the intake of sodium and inorganic phosphorus. Finally, the limited evidence for restrictions on dietary potassium intake is summarized.

Effects of lanthanum carbonate and calcium carbonate on fibroblast growth factor 23 and hepcidin levels in chronic hemodialysis patients.

BACKGROUND: Phosphate binders have an impact on fibroblast growth factor 23 (FGF23); however, the effect of phosphate binders on serum hepcidin has not been explored. We conducted a 24-week multicenter randomized controlled trial to investigate the effects of lanthanum carbonate or calcium carbonate monotherapy on serum phosphate, FGF23, and hepcidin levels in chronic hemodialysis patients. METHODS: Forty-six patients were recruited, and daily dietary phosphorus was controlled between 600-800 mg. Serum calcium, phosphate, albumin, alkaline phosphatase (ALP), FGF23, intact parathyroid hormone (iPTH), hepcidin, high-sensitivity CRP (hsCRP), 25(OH)D, 1,25(OH)2D, fetuin-A, and osteopontin were checked as scheduled. RESULTS: Twenty-five patients completed the study. Mean serum FGF23 level was significantly decreased after a 24-week treatment with lanthanum (8677.5 ± 7490.0 vs. 4692.8 ± 5348.3 pg/mL, p = 0.013, n = 13), but not with calcium (n = 12). The reduction of serum hepcidin in lanthanum group was positively correlated with the decrement of serum phosphate (r = 0.631, p = 0.021) and serum hsCRP (r = 0.670, p = 0.012) levels, respectively. Serum ALP, iPTH, vitamin D, fetuin-A, and osteopontin revealed no significant inter- or intragroup differences. CONCLUSIONS: In summary, a decrease in serum FGF23 levels and a trend of decline in hepcidin levels were observed only in lanthanum group.

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.

Phosphorus Regulation in Chronic Kidney Disease.

Serum phosphorus levels stay relatively constant through the influence of multiple factors-such as parathyroid hormone, fibroblast growth factor 23, and vitamin D-on the kidney, bone, and digestive system. Whereas normal serum phosphorus ranges between 3 mg/dL to 4.5 mg/dL, large cross-sectional studies have shown that even people with normal kidney function are sometimes found to have levels ranging between 1.6 mg/dL and 6.2 mg/dL. While this may partially be due to diet and the factors mentioned above, total understanding of these atypical ranges of serum phosphorus remains uncertain. Risks for bone disease are high in people aged 50 and older, and this group comprises a large proportion of people who also have chronic kidney disease. Consuming diets low in calcium and high in phosphorus, especially foods with phosphate additives, further exacerbates bone turnover. Existing bone disease increases the risk for high serum phosphorus, and higher serum phosphorus has been associated with increased adverse events and cardiovascular-related mortality both in people with chronic kidney disease and in those with no evidence of disease. Once kidney function has deteriorated to end-stage disease (Stage 5), maintaining normal serum phosphorus requires dietary restrictions, phosphate-binding medications, and dialysis. Even so, normal serum phosphorus remains elusive in many patients with Stage 5 kidney disease, and researchers are testing novel targets that may inhibit intestinal transport of phosphorus to achieve better phosphate control. Protecting and monitoring bone health should also aid in controlling serum phosphorus as kidney disease advances.

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.

Effect of a mixture of GOS/FOS® on calcium absorption and retention during recovery from protein malnutrition: experimental model in growing rats.

INTRODUCTION: During growth, protein deprivation impairs epiphyseal growth plate (EGP) height, bone volume (BV) and endochondral ossification. During catch-up growth, Ca availability becomes essential to ensure the extra amount needed to achieve optimal peak bone mass and strength. GOS and FOS improve mineral absorption in the colon. PURPOSE: The effect of a mixture of GOS/FOS® 9:1 added to a 0.5 %Ca (NCa) and a 0.3 %Ca (LCa) diets on Ca, P and Mg absorptions and bone mineralization, density and structure using an experimental model of growing rats recovering from early protein malnutrition was investigated. METHODS: To induce protein malnutrition, rats were fed a low protein diet: 4 % (LPD) during 1 week and then were randomly assigned to recovery groups (R) until day 50 (T = 50) as follows: R0.5 %: NCa; RP0.5 %: NCa + 5.3 % GOS/FOS®; R0.3 %: LCa and RP0.3 %: LCa + 5.3 % GOS/FOS®. Control groups received the 0.5 %Ca or 0.3 %Ca diet from weaning until day 40 or 50. RESULTS: Body weight and length increased in C groups throughout the study; both were arrested in all R during LPD consumption and increased immediately after re-feeding. Independently of dietary Ca content, LS counts, ß-glucosidase and Ca, P and Mg absorption increased, whereas cecum pH, ß-glucuronidase, urease and tryptophanase decreased in RP0.5 %: and RP0.3 %: as compared to the other studied groups (p < 0.01). Prebiotic consumption decreased CTX levels and increased femur Ca, Mg and P contents, total skeleton bone mineral content, proximal tibia and spine BMD, BV, EGP height and hypertrophic zone thickness, stiffness and elastic modulus as compared to recovery groups fed the prebiotic-free diets. CONCLUSION: Under the present experimental conditions, GOS/FOS® mixture induced colonic positive effects, which increased Ca, P and Mg absorption. Thus, consuming the prebiotic-containing diet resulted in an extra amount of minerals that improved bone development in growing rats recovering from protein malnutrition.

Additional benefit of dietitian involvement in dialysis staffs-led diet education on uncontrolled hyperphosphatemia in hemodialysis patients.

BACKGROUND: Sustained adherence to dietary phosphorus (P) restriction recommendations among hemodialysis patients is questionable. The aim of this study was to evaluate the effectiveness of additional diet education delivered by a dietitian on the control of hyperphosphatemia. METHODS: We conducted an 8-month prospective observational study in hemodialysis patients who had uncontrolled hyperphosphatemia. In the first half of the study (experimental) period, the dialysis nurses and physicians provided the routine dietetic education with the control group (n = 31), while the experimental group (n = 30) received the routine dietetic education plus an additional diet education delivered by dietitians. Both groups received the routine dietetic education in the rest of the study period to test whether the improvement of serum P level was sustained. The primary outcomes were changes in serum P level. RESULTS: At baseline, there was no significant difference in serum P levels between groups (P = 0.27). In the experimental period, monthly serum P levels decreased significantly in both groups (P < 0.001) and the magnitudes of reduction were 1.81 ± 1.46 and 0.94 ± 1.33 mg/dL in the experimental and control groups, respectively (P = 0.02), at the end. The experimental group maintained such improvement for one more month (P = 0.02), but faded out over time. CONCLUSION: Renal diet education guided either by dietitians plus dialysis staffs or dialysis staffs alone reduces serum P level and dietitian-guided diet education provides an additional benefit on controlling hyperphosphatemia in hemodialysis patients.