Effect of a plant protein-rich diet on postprandial phosphate metabolism in healthy adult men: a randomised controlled trial.

BACKGROUND: This study examined the effects of animal protein- and plant protein-rich diets on postprandial phosphorus metabolism in healthy male subjects. METHODS: The study was conducted by randomised parallel-group comparison of healthy men aged 21-24 years. In Study 1, participants were divided into two groups and consumed either a 70% animal protein diet (AD, n = 6) or a 70% plant protein diet (PD, n = 6). In Study 2, participants were divided into three groups and consumed either AD (n = 10), PD (n = 10) or AD + DF, a 70% animal protein diet loaded with the same amount of fibre as PD (n = 9). The phosphorus contents of the diets used in this study were nearly equivalent (AD, 710.1 mg; PD, 709.7 mg; AD + DF, 708.9 mg). Blood and urine samples were collected before, and 2 and 4 h after the meal to measure phosphorus and calcium levels. RESULTS: In Study 1, PD consumption resulted in lower blood and urinary phosphorus concentrations 2 h postprandially compared with AD (p < 0.05). In Study 2, blood phosphorus levels in AD + DF after the diet remained lower, but not significantly so compared with AD, and urinary phosphorus levels were significantly lower 2 h postprandially (p < 0.05). CONCLUSIONS: A plant protein-rich diet reduced rapid postprandial increases in blood and urinary phosphorus concentrations compared with the animal protein-rich diets, suggesting that dietary fibre may play a partial role in the postprandial decreases in blood and urinary phosphorus concentrations.

Phosphorus harvesting from fresh human urine: A strategy of precisely recovering high-purity calcium phosphate and insights into the precipitation conversion mechanism.

Phosphorus (P) harvesting from source-separated urine to optimize the overall nutrient loop is one of the most appealing benefits and is a global research interest in wastewater management and treatment. However, current P precipitation is mainly oriented to struvite, which is limited by the issues such as relatively low product purity and high cost of Mg source. Distinguished from previous conventional struvite precipitation, the strategy of precisely harvesting P from fresh human urine as high-purity calcium phosphate was first proposed in this study. This enhanced strategy can optimize P harvesting performance and product purity by simply regulating the consumption of calcium-based materials via model simulation and experimental validation. The thermodynamic model was constructed to probe the precipitation conversion mechanism, and visually predict the component and yield for products under various operating conditions. Batch experiments were conducted to investigate P recovery performance as a function of initial Mg2+ concentration, initial pH level, as well as degree of urine hydrolysis. Moreover, the alternative dosing scheme with different calcium salts and alkali was presented, diversifying the options for efficient P recovery. The results showed that, from the perspective of acidic storage for fresh urine, P recovery can be boosted along with eliminating urine hydrolysis. In urine with an initial pH=2.0, P can be completely recovered and purity for calcium phosphate can be optimized to 100% within a Ca/P ratio range of 1.67-2.3. Overall, this work is of great significance for precisely and efficiently harvesting P from urine and provides an integrated strategy for P resource recovery from urine.

Urinary minerals excretion among primary schoolchildren in Dubai-United Arab Emirates.

INTRODUCTION: Urinary excretion of calcium (Ca), magnesium (Mg), phosphorus (P), iodine and fluoride is used to assess their statuses and/or the existence of metabolic abnormalities. In the United Arab Emirates (UAE), the urinary concentration of these minerals among children have not been documented. MATERIALS AND METHODS: A cross-sectional study, including 593 subjects (232 boys and 361 girls), was conducted among healthy 6 to 11-year-old Emirati children living in Dubai. Non-fasting morning urine samples and anthropometrical measurements were collected and analyzed. Results were expressed as per mg of creatinine (Cr). RESULTS: On average, estimated Cr excretion was 17.88±3.12 mg/kg/d. Mean urinary Ca/Cr, Mg/Cr and P/Cr excretions were 0.08±0.07 mg/mg, 0.09±0.04 mg/mg, and 0.57±0.26 mg/mg respectively. Urinary excretion of Ca, Mg and P were found to decrease as age increased. Urinary excretion and predicted intake of fluoride were lower than 0.05 mg/kg body weight per day. Surprisingly, more than 50% of the children were found to have urinary iodine excretion level above adequate. CONCLUSION: The Emirati schoolchildren had comparable levels of urinary Ca, Mg and P excretion to other countries. The 95% percentile allows the use of the current data as a reference value for the detection of mineral abnormalities. Fluoride excretion implies that Emirati children are at low risk of fluorosis. The level of urinary iodine excretion is slightly higher than recommended and requires close monitoring of the process of salt iodization to avoid the harmful impact of iodine overconsumption.

Dominant factors of the phosphorus regulatory network differ under various dietary phosphate loads in healthy individuals.

BACKGROUND: The purpose of this study was to explore the contribution of each factor of the phosphorus metabolism network following phosphorus diet intervention via Granger causality analysis. METHODS: In this study, a total of six healthy male volunteers were enrolled. All participants sequentially received regular, low-, and high-phosphorus diets. Consumption of each diet lasted for five days, with a 5-day washout period between different diets. Blood and urinary samples were collected on the fifth day of consumption of each diet at 9 time points (00:00, 04:00, 08:00, 10:00, 12:00, 14:00, 16:00, 20:00, 24:00) for measurements of serum levels of phosphate, calcium, PTH, FGF23, BALP, α-Klotho, and 1,25 D and urinary phosphorus excretion. Granger causality and the centrality of the above variables in the phosphorus network were analyzed by pairwise panel Granger causality analysis using the time-series data. RESULTS: The mean age of the participants was 28.5 ± 2.1 years. By using Granger causality analysis, we found that the α-Klotho level had the strongest connection with and played a key role in influencing the other variables. In addition, urinary phosphorus excretion was frequently regulated by other variables in the network of phosphorus metabolism following a regular phosphorus diet. After low-phosphorus diet intervention, serum phosphate affected the other factors the most, and the 1,25 D level was the main outcome factor, while urinary phosphorus excretion was the most strongly associated variable in the network of phosphorus metabolism. After high-phosphorus diet intervention, FGF23 and 1,25 D played a more critical role in active regulation and passive regulation in the Granger causality analysis. CONCLUSIONS: Variations in dietary phosphorus intake led to changes in the central factors involved in phosphorus metabolism.

Intestinal Phosphorus Absorption in Moderate CKD and Healthy Adults Determined Using a Radioisotopic Tracer.

BACKGROUND: Reducing intestinal phosphorus absorption is a cornerstone in CKD-MBD management. Yet, knowledge gaps include how CKD pathophysiology affects intestinal phosphorus absorption. In vivo rodent studies suggest that intestinal phosphorus absorption remains inappropriately normal in early-moderate CKD, despite declining 1,25-dihydroxyvitamin D (1,25D). We measured intestinal phosphorus absorption in patients with moderate CKD versus healthy adults using a direct radiotracer method. METHODS: Patients with CKD and healthy adults matched for age, sex, and race were enrolled in this 8-day controlled diet study: the first 6 days outpatient and the final 2 days inpatient. Oral and intravenous doses of 33P and serial blood and urine sampling determined intestinal phosphorus absorption during the final 2 days. Secondary outcomes included fasting biochemistries and 24-hour urine phosphorus (uP). RESULTS: In total, n=8 patients with CKD (eGFR=29-55 ml/min per 1.73 m2) and n=8 matched healthy controls completed the study. On a controlled diet, no difference in fractional intestinal phosphorus absorption was detected between patients with CKD and healthy adults (0.69 versus 0.62, respectively; P=0.52), and this was similar for 24-hour uP (884 versus 935 mg/d, respectively; P=0.70). Fractional intestinal phosphorus absorption was not significantly related to 24-hour uP. Patients with CKD had higher serum intact PTH and intact FGF23 and lower 1,25D. The relationship between 1,25D and fractional intestinal phosphorus absorption was not statistically significant. CONCLUSIONS: Intestinal phosphorus absorption with typical dietary intake did not differ in patients with moderate CKD compared with controls, despite lower serum 1,25D levels. In this setting, a relationship between 24-hour uP and fractional or absolute intestinal absorption was not evident. Further investigation is needed to determine what factors influence intestinal phosphorus absorption in CKD and the apparent lack of compensation by the intestine to limit phosphorus absorption in the face of declining kidney function and reduced 1,25D. Whether this is evident across a range of dietary phosphorus intakes, as well as CKD severity, also needs to be determined. CLINICAL TRIAL REGISTRY NAME AND REGISTRATION NUMBER: Phosphorus Absorption in Healthy Adults and in Patients with Moderate Chronic Kidney Disease, NCT03108222.

Combination treatment with tenapanor and sevelamer synergistically reduces urinary phosphorus excretion in rats.

The majority of patients with chronic kidney disease (CKD) receiving dialysis do not achieve target serum phosphorus concentrations, despite treatment with phosphate binders. Tenapanor is a nonbinder, sodium/hydrogen exchanger isoform 3 (NHE3) inhibitor that reduces paracellular intestinal phosphate absorption. This preclinical study evaluated the effect of tenapanor and varying doses of sevelamer carbonate on urinary phosphorus excretion, a direct reflection of intestinal phosphate absorption. We measured 24-h urinary phosphorus excretion in male rats assigned to groups dosed orally with vehicle or tenapanor (0.3 mg/kg/day) and provided a diet containing varying amounts of sevelamer [0-3% (wt/wt)]. We also evaluated the effect of the addition of tenapanor or vehicle on 24-h urinary phosphorus excretion to rats on a stable dose of sevelamer [1.5% (wt/wt)]. When administered together, tenapanor and sevelamer decreased urinary phosphorus excretion significantly more than either tenapanor or sevelamer alone across all sevelamer dose levels. The Bliss statistical model of independence indicated that the combination was synergistic. A stable sevelamer dose [1.5% (wt/wt)] reduced mean ± SE urinary phosphorus excretion by 42 ± 3% compared with vehicle; together, tenapanor and sevelamer reduced residual urinary phosphorus excretion by an additional 37 ± 6% (P < 0.05). Although both tenapanor and sevelamer reduce intestinal phosphate absorption individually, administration of tenapanor and sevelamer together results in more pronounced reductions in intestinal phosphate absorption than if either agent is administered alone. Further evaluation of combination tenapanor plus phosphate binder treatment in patients receiving dialysis with hyperphosphatemia is warranted.

MicroRNA-497 elevation or LRG1 knockdown promotes osteoblast proliferation and collagen synthesis in osteoporosis via TGF-ß1/Smads signalling pathway.

MicroRNAs (miRNAs) have been corroborated to engage in the process of cellular activities in osteoporosis. However, few researches have been conducted to expose the integrated role of miR-497, leucine-rich alpha-2-glycoprotein-1 (LRG1) and transforming growth factor beta 1 (TGF-ß1)/Smads signalling pathway in osteoporosis. Thereafter, the study is set out to delve into miR-497/LRG1/TGF-ß1/Smads signalling pathway axis in osteoporosis. Osteoporosis bone tissues and normal bone tissues were collected. Rat osteoporosis models were constructed via ovariectomy. Model rats were injected with restored miR-497 or depleted LRG1 to explore their roles in osteoporosis. Rat osteoblasts were extracted from osteoporosis rats and transfected with restored miR-497 or depleted LRG1 for further verification. MiR-497 and LRG1 expression in femoral head tissues and osteoblasts of osteoporosis rats were detected. TGF-ß1/Smads signalling pathway-related factors were detected. MiR-497 was poorly expressed while LRG1 was highly expressed and TGF-ß1/Smads signalling pathway activation was inhibited in osteoporosis. MiR-497 up-regulation or LRG1 down-regulation activated TGF-ß1/Smads signalling pathway, promoted collagen type 1 synthesis and suppressed oxidative stress in femoral head tissues in osteoporosis. MiR-497 restoration or LRG1 knockdown activated TGF-ß1/Smads signalling pathway, promoted viability and suppressed apoptosis of osteoblasts in osteoporosis. Our study suggests that miR-497 up-regulation or LRG1 down-regulation promotes osteoblast viability and collagen synthesis via activating TGF-ß1/Smads signalling pathway, which may provide a novel reference for osteoporosis treatment.

Effect of a maximal exercise test on serum and urinary concentrations of magnesium, phosphorous, rubidium and strontium in athletes.

AIM: This study aims to determine the changes induced by a maximal exercise test until exhaustion on the serum and urinary concentrations of Magnesium (Mg), Phosphorous (P), Rubidium (Rb) and Strontium (Sr) in athletes (AG) and sedentary students (SG). METHODS: Fifty subjects participated in the study divided into two groups. In AG there were twenty-five male athletes and in SG there were twenty-five male sedentary students. Both groups performed an exercise test until exhaustion, starting at 8 or 10 km/h respectively, and increasing the speed at 1 km/h every 400 m. Serum and urine samples were obtained from all participants before and after the test. RESULTS: Regarding the basal status, AG showed lower values of Mg in serum (p < 0.05) and urine (p < 0.01), but higher concentrations of serum P (p < 0.05) in comparison to SG. Comparing the pre and post-test values, corrected or non-corrected for hemoconcentration in serum and for creatinine in urine, AG showed a decrease in serum Mg (p < 0.05), in serum P (p < 0.01) and in urinary Sr (p < 0.01) while an increase was observed in urinary P (p < 0.05) and in urinary Rb (p < 0.05). CONCLUSIONS: It can be concluded that a treadmill test until exhaustion leads to changes in serum and urinary concentrations of minerals in both AG and SG males. This may reflect an adaptive response of the body to overcome the physical stress and, in some cases, to avoid loss of these elements.

Preliminary analysis of serum electrolytes and body mass index in patients with and without urolithiasis.

OBJECTIVES: To compare body mass index (BMI); serum parameters; and urine parameters between patients with and without urolithiasis. METHODS: Data from 1164 patients admitted to our Department of Urology from January 2011 to July 2013 were retrospectively reviewed; 714 patients (age, 5-87 years; male:female ratio, 1.8:1) exhibited urolithiasis, and 450 patients (age, 12-94 years; male:female ratio, 3.8:1) did not. Blood and urine were collected from patients the morning after hospital admission. Serum and urine parameters were checked by an automatic biochemistry analyzer. Statistical analysis included the Mann-Whitney U test and binary logistic regression. RESULTS: Serum sodium, potassium, chloride, calcium, phosphorus, and carbon dioxide combining power significantly differed between groups. In male patients, serum sodium, calcium, and phosphorus levels were higher in the urolithiasis group, whereas serum potassium and urine pH levels were lower. In female patients, serum sodium was higher in the urolithiasis group. BMI was higher in the urolithiasis group in all patients, male and female. Respective ß-values of serum sodium and BMI in male patients were 0.077 and 0.084; in female patients, these values were 0.119 and 0.102. CONCLUSIONS: Changes in serum sodium and BMI may be involved in the pathogenesis and treatment of urolithiasis.

Hypophosphatemic Hypovitaminosis D Induces Osteomalacia in the Adult Female Rat.

Osteomalacia is a bone-demineralizing disease of adulthood, often caused by hypovitaminosis D. Current animal models of the disease mimic osteomalacia as a consequence of gastric bypass or toxic exposure to metals, but a relevant model of diet-induced osteomalacia is lacking. For that purpose, 7-month-old female Sprague Dawley rats were randomly assigned into 2 weight-stratified groups and maintained for 4 months on synthetic diets containing negligible or normal levels of vitamin D. The dietary regimen resulted in vitamin D deficiency as measured by 25-hydroxyvitamin D serum levels; however, hypovitaminosis D per se did not affect biomarkers of calcium metabolism and bone turnover, nor did it result in increased osteoid. Thus, vitamin D depletion through the diet was found to be insufficient to induce an osteomalacia-like phenotype in the adult rat. After 4 months, the phosphate content of the vitamin D-depleted diet had decreased to 0.16% (calcium:phosphorus ratio of 5.85), resulting in an osteomalacic-like condition (trabecular osteoid surface/bone surface constituted 33%; CI, 26-40). The diet change also affected both metabolic and bone turnover biomarkers, including significantly suppressing serum fibroblast growth factor 23. Furthermore, decreased dietary phosphate in a vitamin D-depleted diet led to microarchitectural changes of trabecular and cortical bone, lower bone mass density, lower bone mass content and decreased bone strength, all indicating reduced bone quality. Taken together, our results show that osteomalacia can be induced in the adult female rat by depleting vitamin D and lowering phosphate content in the diet.

ANALYSIS OF THE INDEXES OF CALCIUM AND PHOSPHORUS EXCHANGE, THE MARKERS OF THEIR REGULATION AND INDEX OF THE ACTIVITY OF SYSTEMIC LUPUS ERYTHEMATOSUS.

In the article we have analyzed the interrelations of the indexes of calcium and phosphor exchange, the markers of their regulation and the indexes of Systemic Lupus Erythematous activity. As a result of an examination of 123 premenopausal women with systemic lupus erythematosus and 25 mostly healthy women at premenopausal status of a relative age it was established that: according to the average values, the indexes of total calcium, ionized calcium, phosphor in the blood, phosphor in the daily urine, parathormone for the patients with Systemic Lupus Erythematous and healthy people did not differ. The content of calcium in the urine was authentically higher, while the content of vitamin D for the patients with Systemic Lupus Erythematous was lower in comparison to the healthy ones. There is a direct authentic connection between the content of calcium in urine and the activity index by SLEDAI that is why it is possible to claim that in case of the decrease of the illness activity the excretion of calcium in kidneys increases. A total index of activity by SLEDAI intercorrelates with the content of vitamin D in blood serum, namely the rise of activity by SLEDAI leads to the decrease of the vitamin D content in the blood serum.

Bone metabolism, bone mass and structural integrity profile in professional male football players.

BACKGROUND: Physical exercise plays an important role in bone mineralization as well as factors involved in bone metabolism influence the athletic performance. In European countries, soccer is the most popular sport. The aim of the study was to investigate bone metabolism, bone mass and structural integrity profile in professional male adult football players. METHODS: Sixteen professional male football players from a single team of the Second division Italian League (mean age 22.4±0.7 years) were enrolled. Bone biochemical parameters, including serum calcium, phosphorus, albumin, creatinine, alkaline phosphatase, intact plasma PTH, 25-hydroxy-vitamin D (25-OHD), 24-h urinary calcium and phosphorus, and calcaneal quantitative ultrasound (QUS), were evaluated at the beginning (October 2012) and at the end of the League (May 2013). RESULTS: 25-OHD levels were significantly lower at the end of the League compared to the beginning (27.1±5.9 vs. 36.6±9.5 ng/mL, fold change [FC]=0.25, P=0.008), and the prevalence of 25-OHD deficiency increased from 25% to 73%. Moreover, higher rate of previous bone, cartilage or ligament injuries correlated with 25-OHD deficiencies (P=0.014). T-score and Z-score were at the upper limits of the normality ranges, without significant difference between the beginning and end of the League. Phosphaturia was slightly decreased at the end of the League (691.0±364.5 vs. 934.0±274.3 mg/24h, FC=0.26, P=0.06). A significant correlation was found between phosphaturia and BQI (R2=0.28, P=0.03), and both T-s and Z-s (R2=0.28, P=0.03) at the beginning of the League. CONCLUSIONS: With this pilot study, we demonstrated that vitamin D status significantly worsened at the end of the League. Therefore, vitamin D supplementation might be suggested in adult football players in order to prevent vitamin D deficiency and improve the athletic performance.

Conventional and novel impacts of ferric citrate on iron deficiency anemia and phosphorus metabolism in rats.

Ferric citrate is an oral iron-based phosphate binder, being known to affect iron status and improve iron deficiency anemia (IDA) in chronic kidney disease (CKD) patients. We examined whether oral administration of ferric citrate could change iron status and improve anemia without affecting phosphorus metabolism in iron deficiency anemia rats. In Normal rat study, normal rats were fed a diet containing 0.3 or 3% ferric citrate for 11 days for setting the dose and administration period of ferric citrate. The effects of ferric citrate on iron status- and phosphorus metabolism-related parameters were evaluated using blood and urine samples. Next, an iron deficiency anemia was induced by feeding iron-depleted diet in rats. After 7 days of starting the iron-depleted diet, 0.3% ferric citrate was administered for 7 days by dietary admixture. Iron status- and phosphorus metabolism-related parameters were evaluated with blood and urine samples. In Normal rat study, 3% ferric citrate treatment increased serum iron level and transferrin saturation (TSAT), and decreased serum phosphorus level, intact fibroblast growth factor 23 (iFGF23) level, and urinary phosphorus excretion, but 0.3% ferric citrate treatment showed no effects. On the other hand, in Iron deficiency anemia rat study, 0.3% ferric citrate treatment increased iron status-related parameters and improved anemia, but did not show any apparent changes in phosphorus metabolism-related parameters. In conclusion, ferric citrate could have hematopoietic effects without affecting phosphorus metabolism, and could be a potential option for the treatment of IDA in patients without CKD.

The recovery of phosphorus from source-separated urine by repeatedly usable magnetic Fe3O4@ZrO2 nanoparticles under acidic conditions.

The separation of urine at source for phosphorus (P) recovery is attractive taking into account the high P concentration and small volume. However, the treatment of urine is still challenging due to its unpleasant odor and hygiene problems. Because the above problems could be solved by acidification to keep the pH of urine below 4, we propose a novel strategy to recover P from acidified urine using tailored hydrous zirconia-coated magnetite nanoparticles (Fe3O4@ZrO2). This strategy involves the selective adsorption of phosphate by easily separable and reusable Fe3O4@ZrO2, the desorption of adsorbed phosphate, and the precipitation of desorbed phosphate as calcium phosphate fertilizer. The results indicated that at pH 4, the P in synthetic urine was selectively adsorbed and could be exhausted using Fe3O4@ZrO2. Nearly all (>97.5%) of the sequestered P on the Fe3O4@ZrO2 nanoparticles was stripped using ≥1 M NaOH solution and ~100% of the stripped P was then successfully transformed into calcium phosphate, upon adding CaCl2 at pH >12 and a Ca/P molar ratio of 3. The liquid/solid (Fe3O4@ZrO2 particles) mixture could be conveniently separated for reuse using an external magnetic field. The reusability of the Fe3O4@ZrO2 nanoparticles in the extraction of P from synthetic urine was confirmed using five cycles of the adsorption-desorption process and their performance validated using real urine samples. The mechanism of phosphate adsorption was investigated using XPS, FTIR and zeta potential measurements, showing that phosphate was chemically adsorbed on the surface through direct coordination to zirconium atom via ligand exchange.

Arctigenin promotes bone formation involving PI3K/Akt/PPARγ signaling pathway.

This study investigated the mechanisms through which arctigenin promotes osteogenesis. Bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (OVX) rats were differentiated into osteoblasts, and osteogenesis was evaluated via Alizarin Red S (ARS) staining and alkaline phosphatase (ALP) measurements in cultured BMSCs. The levels of phosphorylated AKT serine/threonine kinase 1 (p-Akt), and peroxisome proliferator-activated receptor gamma (PPARγ) expression were quantified by Western blot analysis. The levels of urine calcium (U-Ca), urine phosphorus (U-P), serum ALP, and bone mineral density (BMD) of OVX rats were assessed in vivo. The results showed that treatment with arctigenin in rat BMSCs enhanced mineralization, increased ALP activity, increased the expression of Akt and p-Akt, and decreased PPARγ expression, consistent with its ability to promote osteoblast differentiation. Furthermore, arctigenin prevented OVX-induced osteoporosis in rats by increasing BMD and ALP activity and inhibiting the loss of Ca and P. In contrast, treatment with LY294002, a selective inhibitor of the phosphatidylinositol 3-kinase (PI3K), produced the opposite phenotype. These data suggest that the protective effects of arctigenin on BMSCs and OVX rat models result from the induction of osteogenesis involving the PI3K/Akt/PPARγ axis.

[Idiopathic hypercalciuria: can the diuretics be avoided?] / Hipercalciuria idiopática ¿Se pueden evitar los diuréticos?

Idiopathic hypercalciuria is defined as calcium excretion greater than 220 and 300 mg/day in women and men respectively, or greater than 4 mg/kg body weight. In women with osteoporosis it is observed in 19% of cases, while in kidney stones cases varies between 50 and 70%. We selected 206 hypercalciuric patients from our database, with and without renal lithiasis, to whom a restricted diet had been indicated. We divided them, according to the response, into a dependent diet and an independent diet. We considered 122 patients with diagnosis of hypercalciuria diet dependent (105 women and 17 men), which were followed with dietary control (800 mg of calcium, around 1 g of animal proteins and < 100 mEq sodium a day). The appearance of stones, or the recurrence of stones, was not considered, nor was bone involvement. After an average of 17 months, everyone had their calciuria controlled and there were even 16 (13%) who, after 42 months of follow-up, continued to be normocalciuric only on a diet. We conclude that the division of the hypercalciurias is fundamental, according to their response to a restricted diet, in order to avoid or postpone the use of diuretics and its adverse effects, with an adequate management of the diet.

La hipercalciuria idiopática se define como la excreción de calcio superior a 220 y 300 mg/día en mujeres y hombres respectivamente o bien mayor a 4 mg/kg peso. En mujeres con osteoporosis se observa en el 19% de los casos, mientras que en litiasis renal varía entre el 50 y 70%. Seleccionamos 206 pacientes hipercalciúricos, de nuestra base de datos, con y sin litiasis renal, a los que se les había indicado una dieta restringida. Luego los dividimos, de acuerdo a la respuesta, en dieta dependiente y dieta independiente. De estos solo consideramos 122 pacientes con diagnósticos de hipercalciuria dieta-dependiente (105 mujeres y 17 hombres), que fueron seguidos con control dietario (800 mg de calcio, alrededor de 1 g de proteínas animales y < 100 mEq de sodio diarios). No se consideró la aparición de cálculos, o la recurrencia de los mismos, como tampoco el compromiso óseo. Luego de una media de 17 meses todos tenían controlada la calciuria e incluso hubo 16 (13%) que luego de 42 meses de seguimiento persistían normocalciúricos solo con dieta. Concluimos que es fundamental la división de las hipercalciurias, según su respuesta a una dieta restringida, con el fin de evitar o postergar el uso de diuréticos y sus efectos adversos, con una administración adecuada de la dieta.

A Pilot Randomized Crossover Trial Assessing the Safety and Short-Term Effects of Walnut Consumption by Patients with Chronic Kidney Disease.

The aim of this study of patients with chronic kidney disease (CKD) is to assess the safety of daily consumption of walnuts on the physiological levels of phosphorous, potassium, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23), and to assess the short-term benefits of this intervention on risk factors associated with cardiovascular events. This led us to perform a prospective, randomized, crossover, pilot clinical trial examined 13 patients with CKD. Subjects were randomly assigned to a diet of 30 g of walnuts per day or the control diet. After 30 days, each group was given a 30-day washout period, and then switched to the alternate diet for 30 days. Urinary and serum levels of phosphorous and potassium, multiple vascular risk factors, and urinary inositol phosphates (InsPs) were measured at baseline and at the end of the intervention period. Our results showed that the walnut dietary supplement led to reduced blood pressure, LDL cholesterol, and albumin excretion, but had no effect on the physiological levels of phosphorous, potassium, PTH, and FGF23. This is the first report to show that daily consumption of walnuts by patients with CKD does not alter their physiological levels of phosphorous, potassium, PTH, and FGF23 when included in a sodium-, protein-, phosphate-, and potassium-controlled diet, and it could be an effective strategy for reducing cardiovascular risk in patients with CKD.

Hipercalciuria idiopática ¿se pueden evitar los diuróticos? / Idiopathic hypercalciuria: can the diuretics be avoided?

La hipercalciuria idiopática se define como la excreció;n de calcio superior a 220 y 300 mg/día en mujeres y hombres respectivamente o bien mayor a 4 mg/kg peso. En mujeres con osteoporosis se observa en el 19% de los casos, mientras que en litiasis renal varía entre el 50 y 70%. Seleccionamos 206 pacientes hipercalció;ºricos, de nuestra base de datos, con y sin litiasis renal, a los que se les había indicado una dieta restringida. Luego los dividimos, de acuerdo a la respuesta, en dieta dependiente y dieta independiente. De estos solo consideramos 122 pacientes con diagnó;sticos de hipercalciuria dieta-dependiente (105 mujeres y 17 hombres), que fueron seguidos con control dietario (800 mg de calcio, alrededor de 1 g de proteínas animales y < 100 mEq de sodio diarios). No se consideró; la aparició;n de cálculos, o la recurrencia de los mismos, como tampoco el compromiso ó;seo. Luego de una media de 17 meses todos tenían controlada la calciuria e incluso hubo 16 (13%) que luego de 42 meses de seguimiento persistían normocalció;ºricos solo con dieta. Concluimos que es fundamental la divisió;n de las hipercalciurias, segó;ºn su respuesta a una dieta restringida, con el fin de evitar o postergar el uso de diuró;©ticos y sus efectos adversos, con una administració;n adecuada de la dieta.

Idiopathic hypercalciuria is defined as calcium excretion greater than 220 and 300 mg / day in women and men respectively, or greater than 4 mg / kg body weight. In women with osteoporosis it is observed in 19% of cases, while in kidney stones cases varies between 50 and 70%. We selected 206 hypercalciuric patients from our database, with and without renal lithiasis, to whom a restricted diet had been indicated. We divided them, according to the response, into a dependent diet and an independent diet. We considered 122 patients with diagnosis of hypercalciuria diet dependent (105 women and 17 men), which were followed with dietary control (800 mg of calcium, around 1 g of animal proteins and < 100 mEq sodium a day). The appearance of stones, or the recurrence of stones, was not considered, nor was bone involvement. After an average of 17 months, everyone had their calciuria controlled and there were even 16 (13%) who, after 42 months of follow-up, continued to be normocalciuric only on a diet. We conclude that the division of the hypercalciurias is fundamental, according to their response to a restricted diet, in order to avoid or postpone the use of diuretics and its adverse effects, with an adequate management of the diet.

Effect of heat exposure and physical exercise until exhaustion in normothermic and hyperthermic conditions on serum, sweat and urinary concentrations of magnesium and phosphorus.

AIM: The aim of this survey was to ascertain the difference in the levels of Magnesium (Mg) and Phosphorus (P) after an exercise test in normothermia and hyperthermia before and after heat acclimation in comparison to their respective pre-test values. METHODS: Twenty-nine male university students were divided into an Experimental Group (EG) (n = 15) and a Control Group (CG) (n = 14). All of them voluntarily participated in this investigation. Both groups performed an incremental test until exhaustion on a cycloergometer in normothermia (22 °C) and hyperthermia (42 °C). EG underwent 9 sessions of heat acclimation (100 °C) in a sauna (Harvia C105S Logix Combi Control; 3-15 W; Finland). Once the experimental period was completed, all initial measurements were carried out again under identical conditions. Urine and blood samples were obtained before and after each trial. Sweat samples were collected at the end of every test performed in hyperthermia. The samples were frozen at -80 °C until further analysis by ICP-MS. RESULTS: Lower seric Mg levels were observed in both groups at the end of pre-acclimation tests. After acclimation, only EG experimented a decrease of Mg in serum after testing (p < .01). The urinary excretion was unaffected in the pre-acclimated period, but EG experimented an increase in Mg after trials in the post-acclimation evaluation (p < .01). Mg sweat loss decreased significantly after heat acclimation (p < .05). P did not undergo changes, except in its urinary excretion, which was elevated after the normothermia trial in the post-acclimation period (p < .05). CONCLUSIONS: It seems that exercise in hyperthermia altered Mg status but not P homeostasis. Additionally, heat acclimation reduces Mg losses in sweat while increasing its loss in urine. Thus, Mg supplementation should be considered in unacclimated and acclimated subjects if physical exercise is going to be performed in hyperthermic conditions.