Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis

2002 ◽  
Vol 92 (5) ◽  
pp. 2097-2104 ◽  
Author(s):  
Claudia Höhne ◽  
Willehad Boemke ◽  
Nora Schleyer ◽  
Roland C. Francis ◽  
Martin O. Krebs ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Respiratory Alkalosis ◽  
High Sodium ◽  
Low Sodium ◽  
Oxygen Fraction ◽  
Arterial Blood ◽  
Inspiratory Oxygen

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium · kg body wt−1 · day−1) or high-sodium (HS = 7.5 mmol sodium · kg body wt−1 · day−1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial Po 2 34.4 ± 2.1 Torr), plasma pH increased from 7.37 ± 0.01 to 7.48 ± 0.01 ( P < 0.05) because of hyperventilation (arterial Pco 2 25.6 ± 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

Dietary sodium affects systemic and renal hemodynamic response to NO inhibition in healthy humans

1998 ◽  
Vol 274 (5) ◽  
pp. F914-F923 ◽  
Author(s):  
J. N. Bech ◽  
C. B. Nielsen ◽  
P. Ivarsen ◽  
K. T. Jensen ◽  
E. B. Pedersen
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Hemodynamics ◽  
Dietary Sodium ◽  
High Sodium ◽  
High Sodium Intake ◽  
Healthy Humans ◽  
Low Sodium ◽  
Arterial Blood ◽  
Relative Decrease

Animal studies have indicated that increased nitric oxide (NO) synthesis plays a significant role in the renal adaptation to increased sodium intake. To investigate the role of NO during increased sodium intake in humans, we studied the effect of acute, systemic injection of N G-monomethyl-l-arginine (l-NMMA) on renal hemodynamics [glomerular filtration rate and renal plasma flow (GFR and RPF, respectively)], urinary sodium excretion (FENa), systemic hemodynamics [mean arterial blood pressure and heart rate (MAP and HR)], and plasma levels of several vasoactive hormones in 12 healthy subjects during high (250 mmol/day) and low (77 mmol/day) sodium intake in a crossover design. The sodium diets were administered for 5 days before the l-NMMA treatments, in randomized order, with a washout period of 9 days between each diet and l-NMMA treatment. GFR and RPF were measured using the renal clearance of51Cr-labeled EDTA and125I-labeled hippuran by the constant infusion technique in clearance periods of 30-min duration. Two baseline periods were obtained, after whichl-NMMA was given (3 mg/kg over 10 min), and the effect of treatment was followed over the next five clearance periods. During high sodium intake,l-NMMA induced a more pronounced relative decrease in RPF ( P = 0.0417, ANOVA), a more pronounced relative decrease in FENa( P = 0.0032, ANOVA), and a more pronounced relative increase in MAP ( P= 0.0231, ANOVA). During low sodium intake, the effect ofl-NMMA on FENa was abolished. During low sodium intake, l-NMMA induced a sustained drop in plasma renin (31 ± 5 vs. 25 ± 5 μU/ml, P < 0.001), which was not seen during high sodium intake. The data indicate that increased production of NO is an important part of the adaptation to increased dietary sodium intake in healthy humans, with respect to renal hemodynamics, sodium excretion, and the secretion of renin.

scholarly journals Joint association of urinary sodium and potassium excretion with cardiovascular events and mortality: prospective cohort study

BMJ ◽  
2019 ◽  
pp. l772 ◽  
Author(s):  
Martin O’Donnell ◽  
Andrew Mente ◽  
Sumathy Rangarajan ◽  
Matthew J McQueen ◽  
Neil O’Leary ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Cardiovascular Events ◽  
Sodium Intake ◽  
Urinary Sodium ◽  
Potassium Excretion ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium ◽  
Sodium And Potassium

AbstractObjectiveTo evaluate the joint association of sodium and potassium urinary excretion (as surrogate measures of intake) with cardiovascular events and mortality, in the context of current World Health Organization recommendations for daily intake (<2.0 g sodium, >3.5 g potassium) in adults.DesignInternational prospective cohort study.Setting18 high, middle, and low income countries, sampled from urban and rural communities.Participants103 570 people who provided morning fasting urine samples.Main outcome measuresAssociation of estimated 24 hour urinary sodium and potassium excretion (surrogates for intake) with all cause mortality and major cardiovascular events, using multivariable Cox regression. A six category variable for joint sodium and potassium was generated: sodium excretion (low (<3 g/day), moderate (3-5 g/day), and high (>5 g/day) sodium intakes) by potassium excretion (greater/equal or less than median 2.1 g/day).ResultsMean estimated sodium and potassium urinary excretion were 4.93 g/day and 2.12 g/day, respectively. After a median follow-up of 8.2 years, 7884 (6.1%) participants had died or experienced a major cardiovascular event. Increasing urinary sodium excretion was positively associated with increasing potassium excretion (unadjusted r=0.34), and only 0.002% had a concomitant urinary excretion of <2.0 g/day of sodium and >3.5 g/day of potassium. A J-shaped association was observed of sodium excretion and inverse association of potassium excretion with death and cardiovascular events. For joint sodium and potassium excretion categories, the lowest risk of death and cardiovascular events occurred in the group with moderate sodium excretion (3-5 g/day) and higher potassium excretion (21.9% of cohort). Compared with this reference group, the combinations of low potassium with low sodium excretion (hazard ratio 1.23, 1.11 to 1.37; 7.4% of cohort) and low potassium with high sodium excretion (1.21, 1.11 to 1.32; 13.8% of cohort) were associated with the highest risk, followed by low sodium excretion (1.19, 1.02 to 1.38; 3.3% of cohort) and high sodium excretion (1.10, 1.02 to 1.18; 29.6% of cohort) among those with potassium excretion greater than the median. Higher potassium excretion attenuated the increased cardiovascular risk associated with high sodium excretion (P for interaction=0.007).ConclusionsThese findings suggest that the simultaneous target of low sodium intake (<2 g/day) with high potassium intake (>3.5 g/day) is extremely uncommon. Combined moderate sodium intake (3-5 g/day) with high potassium intake is associated with the lowest risk of mortality and cardiovascular events.

Abstract P252: The Effects of Sodium Reduction on Metabolism and Thirst

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Stephen P Juraschek ◽  
Edgar R Miller ◽  
Alexander Chang ◽  
Cheryl Anderson ◽  
John E Hall ◽  
...  
Keyword(s):  
Energy Intake ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Control Diet ◽  
Urine Volume ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
High Sodium ◽  
Low Sodium ◽  
Serum Aldosterone

Background: Recent studies challenge the traditional understanding of sodium physiology. Some animal studies suggest that high sodium intake may induce catabolism, leading to weight loss. Other studies suggest that high sodium intake might reduce, rather than increase, thirst. Hypothesis: Higher sodium intake increases thirst, fluid intake, and sodium excretion without altering energy intake or lowering weight. Methods: In the DASH-Sodium feeding study, adults with pre- or stage 1 hypertension without antihypertensive medications, were randomly assigned to the DASH diet or a control diet. On their assigned diet, participants consumed each of three sodium levels for 4 weeks (randomized crossover design). Participants were provided all meals, but could drink water freely. Throughout the trial, calorie intake was adjusted to keep weight constant. The three sodium levels (at 2100 kcal/d) were: low (1150 mg), medium (2300 mg), and high (3450 mg). Weight, energy intake, self-reported thirst, urine volume, plasma renin, serum aldosterone, urine osmolality, and urine sodium excretion were assessed at the end of each period. Results: Among 412 participants (57% women, 57% black, mean age 48 yrs), weight increased slightly with higher sodium on the control diet, but not the DASH diet; energy intake did not vary across sodium levels in both diets ( P -trends > 0.34) ( Table ). In contrast, participants reported more thirst with high vs low sodium (both diets P -trends < 0.001) and potentially higher fluid intake (urine volume) during the control diet (1,566 vs 1,491 ml on high vs low sodium; P -trend = 0.07). On both diets, plasma renin and serum aldosterone were lower with higher sodium (each P -trend < 0.001). Likewise, both urine osmolality and sodium excretion were higher with higher sodium intake (all P -trends < 0.001). Conclusions: Higher sodium intake did not alter energy intake, but did increase thirst and sodium excretion. These findings are consistent with the traditional understanding of the physiology of excess dietary sodium intake.

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

2008 ◽  
Vol 294 (1) ◽  
pp. R17-R25 ◽  
Author(s):  
Mads Kjolby ◽  
Peter Bie
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Ang Ii ◽  
Low Sodium ◽  
Arterial Blood ◽  
Body Sodium ◽  
Custom Made ◽  
Total Body

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03–0.75 mmol·kg−1·day−1for 7 days. Acute NaCl administration increased PV (+6.3–8.9%) and plasma sodium concentration (∼2%) and decreased plasma protein concentration (−6.4–8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.

Increased Renal Sensitivity to Aldosterone in the Potassium-Loaded Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder
Keyword(s):  
Sodium Intake ◽  
Control Diet ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High K ◽  
And Control

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.

Abstract P614: Relationship Of Sodium Intake And Stress With Bone Health In Women

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Allison Jasti ◽  
Deborah L Stewart ◽  
Gregory A Harshfield
Keyword(s):  
Bone Health ◽  
Salt Intake ◽  
Sodium Intake ◽  
Target Organ Damage ◽  
African American Adolescents ◽  
Ang Ii ◽  
Mineral Density ◽  
High Sodium ◽  
Low Sodium ◽  
Relationship Of

Background: The skeleton is vital to sodium homeostasis, accounting for 40% of the body’s sodium. Research indicates stress and low sodium intake are independently associated with RAAS activation. In certain populations, stress can induce salt sensitivity, increasing the risk of hypertension and target organ damage, but the association of low versus high sodium intake with bone health is controversial. Purpose: This study sought out the relationship of low sodium and stress-induced RAAS activation with bone health. The tested hypothesis was those with lowest sodium intake would have lower total bone mineral density (TBMD) and content (TBMC) associated with stress-induced increases in angiotensin ii (Ang II) and aldosterone (Aldo). Methods: We compared effect of stress on Ang II, Aldo, TBMD and TMBC in healthy Caucasian and African-American adolescents. Subjects were grouped by quartiles based on sodium intake, assessed by urinary sodium excretion. Results: Due to females, overall significant inverse associations are observed between TBMD, TBMC, Ang II and Aldo in the lowest sodium intake quartile. Post-stress, women in the lowest sodium intake quartile showed that increases in both Ang II and Aldo correspond with lower TMBC and TMBD. There was no significance between Ang II, Aldo, TMBC and TMBD in the three highest quartiles of women nor in any male quartile. Conclusion: These data suggest Ang II and Aldo may reduce TMBC and TMBD in women. Stress-induced increases in Ang II and Aldo, with low sodium intake, may further reduce TBMD and TBMC in women. Ang II inhibition and/or moderated salt intake may be an efficacious prevention or treatment against the development of osteoporosis.

scholarly journals Urine Spot Samples Can Be Used to Estimate 24-Hour Urinary Sodium Excretion in Children

2018 ◽  
Vol 148 (12) ◽  
pp. 1946-1953 ◽  
Author(s):  
Magali Rios-Leyvraz ◽  
Pascal Bovet ◽  
René Tabin ◽  
Bernard Genin ◽  
Michel Russo ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Population Level ◽  
Urinary Sodium Excretion ◽  
Cross Sectional Study ◽  
Urinary Sodium ◽  
Cross Sectional ◽  
High Sodium ◽  
Individual Level

ABSTRACT Background The gold standard to assess salt intake is 24-h urine collections. Use of a urine spot sample can be a simpler alternative, especially when the goal is to assess sodium intake at the population level. Several equations to estimate 24-h urinary sodium excretion from urine spot samples have been tested in adults, but not in children. Objective The objective of this study was to assess the ability of several equations and urine spot samples to estimate 24-h urinary sodium excretion in children. Methods A cross-sectional study of children between 6 and 16 y of age was conducted. Each child collected one 24-h urine sample and 3 timed urine spot samples, i.e., evening (last void before going to bed), overnight (first void in the morning), and morning (second void in the morning). Eight equations (i.e., Kawasaki, Tanaka, Remer, Mage, Brown with and without potassium, Toft, and Meng) were used to estimate 24-h urinary sodium excretion. The estimates from the different spot samples and equations were compared with the measured excretion through the use of several statistics. Results Among the 101 children recruited, 86 had a complete 24-h urine collection and were included in the analysis (mean age: 10.5 y). The mean measured 24-h urinary sodium excretion was 2.5 g (range: 0.8–6.4 g). The different spot samples and equations provided highly heterogeneous estimates of the 24-h urinary sodium excretion. The overnight spot samples with the Tanaka and Brown equations provided the most accurate estimates (mean bias: −0.20 to −0.12 g; correlation: 0.48–0.53; precision: 69.7–76.5%; sensitivity: 76.9–81.6%; specificity: 66.7%; and misclassification: 23.0–27.7%). The other equations, irrespective of the timing of the spot, provided less accurate estimates. Conclusions Urine spot samples, with selected equations, might provide accurate estimates of the 24-h sodium excretion in children at a population level. At an individual level, they could be used to identify children with high sodium excretion. This study was registered at clinicaltrials.gov as NCT02900261.

Renal and cardiac oxidative/nitrosative stress in salt-loaded pregnant rat

2007 ◽  
Vol 293 (4) ◽  
pp. R1657-R1665 ◽  
Author(s):  
Annie Beauséjour ◽  
Véronique Houde ◽  
Karine Bibeau ◽  
Rébecca Gaudet ◽  
Jean St-Louis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitrosative Stress ◽  
Gestational Hypertension ◽  
Sodium Intake ◽  
Pregnant Rats ◽  
High Sodium ◽  
High Sodium Intake ◽  
Arterial Blood ◽  
Cardiac Ventricle

Sodium supplementation given for 1 wk to nonpregnant rats induces changes that are adequate to maintain renal and circulatory homeostasis as well as arterial blood pressure. However, in pregnant rats, proteinuria, fetal growth restriction, and placental oxidative stress are observed. Moreover, the decrease in blood pressure and expansion of circulatory volume, normally associated with pregnancy, are prevented by high-sodium intake. We hypothesized that, in these pregnant rats, a loss of the balance between prooxidation and antioxidation, particularly in kidneys and heart, disturbs the normal course of pregnancy and leads to manifestations such as gestational hypertension. We thus investigated the presence of oxidative/nitrosative stress in heart and kidneys following high-sodium intake in pregnant rats. Markers of this stress [8-isoprostaglandin F2α (8-iso-PGF2α) and nitrotyrosine], producer of nitric oxide [nitric oxide synthases (NOSs)], and antioxidants [superoxide dismutase (SOD) and catalase] were measured. Then, molecules (Na+-K+-ATPase and aconitase) or process [apoptosis (Bax and Bcl-2), inflammation (monocyte chemoattractant protein-1, connective tissue growth factor, and TNF-α)] susceptible to free radicals was determined. In kidneys from pregnant rats on 1.8% NaCl-water, NOSs, apoptotic index, and nitrotyrosine expression were increased, whereas Na+-K+-ATPase mRNA and activity were decreased. In the left cardiac ventricle of these rats, heightened nitrotyrosine, 8-iso-PGF2α, and catalase activity together with reduced endothelial NOS protein expression and SOD and aconitase activities were observed. These findings suggest that oxidative/nitrosative stress in kidney and left cardiac ventricle destabilizes the normal course of pregnancy and could lead to gestational hypertension.

scholarly journals Sodium Sensitivity, Sodium Resistance, and Incidence of Hypertension

Hypertension ◽  
2021 ◽  
Author(s):  
Jiang He ◽  
Jian-Feng Huang ◽  
Changwei Li ◽  
Jing Chen ◽  
Xiangfeng Lu ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Experimental Studies ◽  
Dietary Sodium ◽  
Cross Sectional ◽  
Incident Hypertension ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
Sodium Diet ◽  
Low Sodium ◽  
Increased Risk

Cross-sectional studies have reported that high sodium sensitivity is more common among individuals with hypertension. Experimental studies have also reported various animal models with sodium-resistant hypertension. It is unknown, however, whether sodium sensitivity and resistance precede the development of hypertension. We conducted a feeding study, including a 7-day low-sodium diet (1180 mg/day) followed by a 7-day high-sodium diet (7081 mg/day), among 1718 Chinese adults with blood pressure (BP) <140/90 mm Hg. We longitudinally followed them over an average of 7.4 years. Three BP measurements and 24-hour urinary sodium excretion were obtained on each of 3 days during baseline observation, low-sodium and high-sodium interventions, and 2 follow-up studies. Three trajectories of BP responses to dietary sodium intake were identified using latent trajectory analysis. Mean (SD) changes in systolic BP were −13.7 (5.5), −4.9 (3.0), and 2.4 (3.0) mm Hg during the low-sodium intervention and 11.2 (5.3), 4.4 (4.1), and −0.2 (4.1) mm Hg during the high-sodium intervention ( P <0.001 for group differences) in high sodium-sensitive, moderate sodium-sensitive, and sodium-resistant groups, respectively. Compared with individuals with moderate sodium sensitivity, multiple-adjusted odds ratios (95% CIs) for incident hypertension were 1.43 (1.03–1.98) for those with high sodium sensitivity and 1.43 (1.03–1.99) for those with sodium resistance ( P =0.006 for nonlinear trend). Furthermore, a J-shaped association between systolic BP responses to sodium intake and incident hypertension was identified ( P <0.001). Similar results were observed for diastolic BP. Our study indicates that individuals with either high sodium sensitivity or sodium resistance are at an increased risk for developing hypertension.

Abstract MP01: Effect Of The DASH-Sodium Diet On Serum Biomarkers Of Inflammation And Mineral Metabolism

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Valerie K Sullivan ◽  
Lawrence J Appel ◽  
Jesse C Seegmiller ◽  
Casey M Rebholz
Keyword(s):  
Mineral Metabolism ◽  
Sodium Intake ◽  
Random Sequence ◽  
Control Diet ◽  
Fibroblast Growth Factor 23 ◽  
Serum Samples ◽  
Urokinase Plasminogen Activator Receptor ◽  
Dash Diet ◽  
High Sodium ◽  
Low Sodium

Background: The blood pressure-lowering effects of the Dietary Approaches to Stop Hypertension (DASH) dietary pattern and reduced sodium intake are well-established. The effects on other biomarkers related to vascular health are of interest and may assist in explaining cardiovascular benefits of the DASH diet. Objective: We hypothesized that a low-sodium DASH diet improves biomarkers of inflammation [i.e. reduces C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR)] and mineral metabolism [phosphorus and fibroblast growth factor-23 (FGF23)]. Methods: We conducted a post hoc analysis of the DASH-Sodium trial using stored frozen serum samples. This controlled feeding study randomized 412 adults to consume either a DASH diet or control diet representative of a typical American diet. Within each arm, participants received three sodium levels (low, intermediate, high) in random sequence, each for 30 days. To maximize contrast, samples collected at the end of the low-sodium DASH (n=198) and high-sodium control (n=194) diets were compared. Between-diet differences in biomarker concentrations were assessed by t-test or Wilcoxon rank sum test for normally distributed and skewed variables, respectively. Results: CRP concentrations did not differ between groups ( P =0.19), but suPAR was higher after the low-sodium DASH diet than the high-sodium control (median, IQR: 2473, 2127-2887 pg/mL vs. 2281, 1929-2679 pg/mL; P =0.003). FGF23 was also higher after the DASH diet (35.9, 26.9-44.8 pg/mL vs. 30.2, 23.5-37.5 pg/mL; P< 0.001). Serum phosphorus was higher after the DASH diet (mean±SEM: 3.5±0.04 mg/dL) versus the control (3.4±0.04 mg/dL; P =0.02). Conclusions: Contrary to our hypothesis, biomarkers of inflammation and mineral metabolism were increased or unchanged by a low-sodium DASH diet compared to a high-sodium control diet. Potential reasons (e.g. short duration of the trial, sodium-specific effects, bioavailable phosphorus-rich dairy intake) require further investigation.

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