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High dietary phosphorus intake (P-In) and high acid loads may adversely affect kidney function. In animal models, excessive phosphorus intake causes renal injury, which, in humans, is also inducible by chronic metabolic acidosis. We thus examined whether habitually high P-In and endogenous acid production during childhood and adolescence may be early indicators of incipient renal inflammatory processes later in adulthood. P-In and acid-base status were longitudinally and exclusively determined by biomarker-based assessment in 277 healthy children, utilizing phosphate and net acid excretion (NAE) measurements in 24 h urine samples repeatedly collected between the ages of 3 and 17 years. Standard deviation scores (by sex and age) were calculated for anthropometric data and for the urinary biomarkers available within age range 3-17 years. Multivariable linear regression was used to analyze the relations of phosphate excretion and NAE with the adulthood outcome circulating interleukin-18 (IL-18), a marker of inflammation and kidney dysfunction. After adjusting for growth- and adulthood-related covariates and pro-inflammatory biomarkers to rule out confounding by non-renal inflammatory processes, regression models revealed a significant positive relationship of long-term NAE ( p = 0.01), but not of long-term phosphate excretion with adult serum IL-18. Similar significant positive regression results were obtained after replacing NAE with 24 h urinary ammonium excretion as the exposition variable. Our results suggest that even moderate elevations in renal ammonia production, as caused by habitually higher acid loading during growth, may affect the intrarenal pro-inflammatory system in the long-term, known to be boosted by acidosis-induced raised ammoniagenesis.

A lower 24-h urine pH (24h-pH), i.e., a higher renal excretion of free protons, at a given acid load to the body, denotes a reduction in the kidney's capacity for net acid excretion (NAE). There is increasing evidence, not only for patients with type 2 diabetes but also for healthy individuals, that higher body fatness or waist circumference (WC) has a negative impact on renal function to excrete acids (NAE). We hypothesized that adiposity-related inflammation molecules might mediate this relation between adiposity and renal acid excretion function. Twelve biomarkers of inflammation were measured in fasting blood samples from 162 adult participants (18-25 yr old) of the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) study who had undergone anthropometric measurements and collected 24-h urine samples. Both Baron and Kenny's (B&K's) steps to test mediation and causal mediation analysis were conducted to examine the potential mediatory roles of biomarkers of inflammation in the WC-24-h pH relationship after strictly controlling for laboratory-measured NAE. In B&K's mediation analysis, leptin, soluble intercellular adhesion molecule 1 (sICAM-1), and adiponectin significantly associated with the outcome 24-h pH and attenuated the WC-pH relation. In agreement herewith, causal mediation analysis estimated the "natural indirect effects" of WC on 24-h pH via leptin ( P = 0.01) and adiponectin ( P = 0.03) to be significant, with a trend for sICAM-1 ( P = 0.09). The calculated proportions mediated by leptin, adiponectin, and sICAM-1 were 64%, 23%, and 12%, respectively. Both mediation analyses identified an inflammatory cytokine (leptin) and an anti-inflammatory cytokine (adiponectin) along with sICAM-1 as being potentially involved in mediating adiposity-related influences on renal acid excretion capacity.

Background: Overweight and higher BMI are known to be related to increased blood pressure (BP) and additionally associate with lowered urine pH values even at comparable total daily acid loading. Since a reduced urine pH level at a given total acid load indicates an impaired renal net acid excretion capacity (NAEC) and renal function also relates to BP, we hypothesized that NAEC may be one mediator of the body fat-BP association., Methods: Ammonium, titratable acid, pH, creatinine, and urea were measured in 24-h urine samples among 9-15-year-old adolescents of the DONALD Study. NAEC was determined as residual of the body surface area-corrected net acid excretion on urine pH (NAEC1) or body surface area-corrected ammonium excretion on urine pH (NAEC2). Markers of body fatness were determined anthropometrically and systolic and diastolic BP sphygmomanometrically. Multilinear regressions were used to examine cross-sectionally the body fat-NAEC and prospectively the NAEC1-BP associations., Results: All body fat parameters were inversely associated with both NAEC1 and NAEC2 among youth (P ≤ 0.01). In a separate prospective analyses, to check for possible mediation, higher adolescent NAEC1 was significantly associated with lower systolic BP in male adults only (P = 0.04), but this association was attenuated to a trend (P = 0.07) in multivariable-adjusted models., Conclusions: Independent of systemic acid load, NAEC, i.e., the kidney's function to eliminate acids is reduced with higher body fatness, and may also contribute as a mediator in the body fatness-BP relation.

Background: Reduced net acid excretion (NAE) capacity indicates a decrease in renal function. This reduction manifests as a disproportionally low 24-h urine pH in relation to the sum of actually excreted ammonium and titratable acidity by the kidney., Objective: The aim of this study was to test the hypothesis that higher body fatness is one determinant of kidney function impairment with a lowered urine pH even at a young age., Methods: NAE, pH, urea, and creatinine were measured in 24-h urine samples from 524 healthy children and adolescents (aged 6-17 y) participating in the DOrtmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study. Body fatness was assessed anthropometrically by body mass index-standard deviation score (BMI-SDS), fat mass index (FMI), body fat % (BF%), and waist circumference (WC). Multivariable linear and mixed linear regressions were used to examine cross-sectionally (n = 524 urine samples; age groups: 6-8, 9-11, 12-14, 15-17 y) and longitudinally (n = 1999 urine samples) the associations of body fatness with 24-h urine pH as the outcome variable, respectively., Results: After adjusting for the kidneys' total net acid load (24-h urinary NAE) and further relevant covariates, FMI showed significant inverse relations with urinary pH in all 4 age groups, and BMI-SDS, BF%, and WC each in 3 out of these 4 groups (P ≤ 0.02). Longitudinal results substantiated these interindividual relations and further showed intraindividual increases in body fatness to be paralleled by urine pH decreases (P ≤ 0.0002)., Conclusions: Independent of underlying acid load, an early increase in body fatness is associated with increased free proton excretion, and thus with a decline in the kidney's acid excretion function, which could potentiate the risk of renal nephrolithiasis., (Copyright © American Society for Nutrition 2019.)

Experimental data and observational studies in adults suggest that even subtle changes in acid-base balance, indicative of a higher systemic proton load, are related to higher blood pressure (BP) levels and an increased hypertension risk. However, these associations have not been investigated during growth. The kidney is the central organ in regulating excretion of nonvolatile acids, and renal citrate excretion has been shown to be a sensitive, noninvasive marker of changes in systemic acid balance. We thus analyzed the prospective relation of 24-h citrate excretion, as well as net acid excretion capacity (NAEC; a noninvasive indicator of the renal ability to excrete protons), during adolescence (boys: 10-15 yr; girls: 9-14 yr) with BP levels in young adulthood (18-30 yr) in 374 healthy participants of the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study. In linear-regression analyses adjusted for age, sex, 24-h urinary excretions of sodium and potassium, as well as further relevant confounders, a 1-mmol/1.73 m 2 /day higher adolescent citrate excretion was related to 1.2 mmHg lower systolic BP ( P = 0.02) but not to diastolic BP ( P = 0.6). A 10-mEq higher NAEC during adolescence was related to 1.7 mmHg lower systolic BP in young men, but this association was statistically nonsignificant ( P = 0.07) after multivariable adjustment. Additional adjustment for adult body mass index did not alter these findings. To conclude, subtle changes in systemic acid-base balance during adolescence are already indicative for later BP. Potential sex differences in these associations should be investigated in further studies.

Metabolic acidosis induces elevated glucocorticoid (GC) levels. However, the influence of less strong daily acid loads on GCs is largely unexplored. To investigate this, we studied whether higher acid loads in children, fully within the normal range of habitual diets, associate with endogenous GCs. In a specific quasi-experimental design, we examined 200 6- to 10-year-old healthy participants of the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study equally divided to either high or low 24-hour renal net acid excretion. Major urinary GC metabolites were analyzed by gas chromatography-mass spectrometry to assess daily adrenal GC secretion and metabolites of tissue cortisol catabolism (6β-hydroxycortisol and 20α-dihydrocortisol). Liquid chromatography-mass spectrometry was used to quantify urinary free cortisol and cortisone. After confounder adjustment, significant positive associations were unmasked for urinary potential renal acid load and net acid excretion with adrenal GC secretion, free cortisone, free cortisone plus cortisol, 6β-hydroxycortisol, and 20α-dihydrocortisol. An inverse association emerged for an enzymatic marker (5β-reductase) of irreversible GC inactivation. Our data suggest that existing moderate elevations in diet-dependent acid loads suffice to raise GCs and affect cortisol metabolism. Thus, potential detrimental effects of high acid loading appear to be mediated, in part, by increased GC activity via increased GC secretion and/or reduced GC inactivation. Higher cortisone levels, directly available for intracrine activation to cortisol may play a special role., (Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Reduced bone mineral density (BMD) and bone mass have been observed in children with idiopathic hypercalciuria. Whether urinary calcium excretion at the higher end of the normal physiologic range can influence bone health in healthy children independent of dietary intake is unknown. Urinary calcium was quantified in 603 24-h urine samples from 154 healthy children and adolescents who had ≥3 urine collections and parallel 3-day weighed dietary records during the 4years preceding proximal forearm bone analyses by peripheral quantitative computed tomography (pQCT). Urinary potential renal acid load (uPRAL) was determined according to urine ionogram by subtracting measured quantitatively important mineral cations from nonbicarbonate anions. Urinary calcium excretion was significantly associated with volumetric (v)BMD (P=0.04), almost significantly with cortical bone mineral content (BMC) (P=0.05), but not with cortical cross-sectional area (CSA) (P=0.09), total CSA (P=0.3), or Strength-Strain Index (P=0.8) in the total population sample. Stratified analyses based on the median split of uPRAL showed that calcium excretion was negatively associated with vBMD (P=0.007), cortical BMC (P=0.001), and cortical CSA (P=0.004) in those children with higher uPRALs, but not in those with low uPRALs (P>0.3). In conclusion, long-term higher calciuria within the physiological range predicts reduced diaphyseal bone mass and bone density particularly in healthy children and adolescents with long-term unfavorable higher dietary acid load, i.e., with lower fruit and vegetable intake., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Nonalcoholic fatty liver disease (NAFLD), frequently already present in young subjects, has been linked to reduced growth hormone levels and signaling. Similar hormonal changes occur during metabolic acidosis (MA), which may thus contribute to an increased NAFLD risk. Because subclinical MA can be diet induced, we aimed to examine whether a higher diet-dependent acid load during adolescence is prospectively associated with several currently used NAFLD surrogates in young adulthood. Dietary acidity during adolescence (boys:10-15 y, girls: 9-14 y) was calculated as potential renal acid load (PRAL) from at least three 3-d weighed dietary records according to a published algorithm considering dietary protein and minerals in 145 healthy participants. Routine measurements derived from blood analysis and anthropometric data in participants' young adulthood (18-25 y) were used to determine the NAFLD surrogates alanine-aminotransferase (ALT), hepatic steatosis index (HSI), and fatty liver index (FLI). Sex-stratified linear regression models, adjusted for dietary fiber, saturated fat, protein, and adolescent BMI SD scores, were run with PRAL as the independent variable. Dietary PRAL during puberty was positively associated with ALT (P = 0.02), HSI (P = 0.002), and FLI (P = 0.005) in adult females but not males. Females with an adolescent dietary acid load in the highest tertile had 3.5, 4.4, and 4.5 higher values of ALT, HSI, and FLI as adults, respectively, compared to females with the lowest PRAL. The present findings suggest that higher dietary acidity in adolescence may be prospectively associated with hepatic lipid accumulation in females. Whether this relationship is due to the higher proton load or rather represents an unhealthy dietary pattern requires further investigation.

In patients with hypercortisolism, who are frequently obese, the prevalence of elevated urinary excretion rates of the potential lithogenic factors (calcium, oxalate, and uric acid) is increased. We examined whether the 24-hour urinary excretion rates of calcium, oxalate, and uric acid are already associated with body fat and endogenous glucocorticoids in healthy free-living children, taking relevant nutritional and acid-base factors into account. Urinary analyte excretions were determined in 24-hour urine samples of 300 healthy children aged 4 to 14 years. Potentially bioactive free glucocorticoids were assessed as urinary free cortisol + urinary free cortisone. Associations of glucocorticoids and percentage body fat with the outcome variables were examined in regression models adjusted for sex, height, growth velocity, urinary volume, net acid excretion, and relevant nutritional factors. Percentage body fat and urinary free cortisol + urinary free cortisone explained most of the growth-independent variation of urinary uric acid and also a relevant part of oxalate, but none of calcium. Net acid excretion, an indicator of endogenous acid production, and dietary protein, salt, and fiber intakes were also variably associated with the outcomes urinary calcium, oxalate, and uric acid. In conclusion, body fatness and potentially bioactive free glucocorticoids (even in the physiologic range) appear to affect urinary excretion rates of oxalate and uric acid, whereas urinary calcium output is more strongly related to dietary factors in healthy children. Our data provide the first in vivo-based evidence that the obesity- or hypercortisolism-associated urolithiasis may be a pathophysiologic continuation of the corresponding endocrine metabolic variations in healthy children.

Alterations in glucocorticoid (GC) metabolism may contribute to the development of obesity and insulin resistance. We aimed to study the role of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in human adiposity, paying special attention to the association between altered GC metabolism and insulin sensitivity. In 24-h urine samples of 72 extremely obese (mean BMI 45.5 +/- 1.1 kg/m(2)), but otherwise healthy patients urinary free cortisol (UFF), urinary free cortisone (UFE), tetrahydrocortisol (THF), 5alpha-tetrahydrocortisol (5alpha-THF), and tetrahydrocortisone (THE) were quantified by radioimmunoassay. The sum of the three major tetrahydrometabolites is an estimate for daily GC secretion, and the sum of UFF and UFE represents potentially bioactive-free-GCs. Thirty healthy lean subjects (BMI 22.3 +/- 0.3 kg/m(2)) served as controls. In obese subjects, absolute daily GC secretion and the potentially bioactive-free-GCs were significantly (P < 0.005) higher than in lean controls (11.8 +/- 0.7 vs. 8.0 +/- 0.6 mg/d; and 171.8 +/- 11.2 vs. 117.6 +/- 9.2 mug/d, respectively). However, when these values were corrected for body surface area (BSA), significant differences were no longer detectable. While enzyme activity indices for 5alpha-reductase and 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) were similar in lean and obese subjects, 11beta-HSD2 was markedly elevated in adiposity (3.7 +/- 0.2 vs. 2.1 +/- 0.1; P < 0.0001). This increase was accompanied by a significant reduction in UFF excretion corrected for BSA (16.5 +/- 1.2 vs. 21.7 +/- 2.0 mug/d/m(2); P = 0.0222). Besides, 11beta-HSD2 activity was significantly correlated with insulin sensitivity (P = 0.0262). When body size is accounted for, both adrenal GC secretion and potentially bioactive-free-GCs are indistinguishable between lean and extremely obese subjects. However in obesity, the kidney appears to intensify its supply of the direct substrate cortisone for extrarenal 11beta-HSD1, which may fuel visceral adiposity and insulin resistance.

Objective: The impact of acid-base balance on health is widely accepted. Here, we describe the potential renal acid load (PRAL) in the diet of healthy German children and adolescents., Design: The Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study is an ongoing longitudinal (open cohort) study (start 1985) collecting detailed data on diet, growth, development and metabolism in infants, children and adolescents., Setting: Research Institute of Child Nutrition, Dortmund., Subjects: Seven hundred and twenty children and adolescents (351 boys and 369 girls), aged 3-18 years, provided 4187 yearly collected 3-day dietary records between 1995 and 2005., Results: Mean daily PRAL was positive in all age/sex groups (6-21 mEq day-1), and significantly higher in boys than in girls after the age of 8 years, even when calculated as mEq MJ-1. Fruits, vegetables and potatoes had a negative impact on PRAL; cheese, dairy products, cereals/bread and meat/fish/eggs had a positive impact. In a mixed linear model, PRAL, expressed as mEq day-1 and mEq MJ-1, remained stable during the study period, since time trends of PRAL-relevant food groups countervail each other. PRAL intake (mEq MJ-1) was significantly positively associated (P < 0.0001) with fat intake (% of energy intake, %E), but negatively with carbohydrate intake (%E; P < 0.0001)., Conclusions: The analysis of dietary habits in our sample of German children and adolescents showed a moderate excess of acidity. Especially older boys should be encouraged to eat more potatoes and vegetables as good sources of dietary alkalinity. The PRAL concept is compatible with current concepts for a healthy diet.

Primarily experimental evidence suggests that endogenous glucocorticoids may be suppressed by adipocyte-derived leptin and elevated by dietary acidity. Therefore, we examined whether these factors may also be relevant in healthy adults on unrestricted diets. For this we used a new methodological approach in which potentially bioactive free glucocorticoids were determined as the sum of urinary free cortisol and urinary free cortisone and that also takes into account total adrenal glucocorticoid secretion assessed by the sum of the 3 major urinary glucocorticoid metabolites tetrahydrocortisone, tetrahydrocortisol, and 5alpha-tetrahydrocortisol. Body composition, plasma cortisol, plasma leptin, and 24-h urinary excretion rates of net acid and glucocorticoid metabolites were examined cross-sectionally in 30 healthy adults (15 women; 22-44 y old; BMI 20-25 kg/m2). Plasma leptin, percentage body fat, and body surface area-corrected adrenal glucocorticoid secretion showed the usual sex dimorphism (male vs. female, P < 0.05 in each case: 2.8 +/- 1.6 microg/L vs. 7.6 +/- 4.9 microg/L, 16.8 +/- 4.2% vs. 26.9 +/- 4.9%, and 5.1 +/- 1.6 mg x m(-2) x d(-1) vs. 4.0 +/- 1.3 mg x m(-2) x d(-1), respectively), whereas net acid excretion, plasma cortisol, and potentially bioactive free glucocorticoids did not differ between the sexes. Potentially bioactive free glucocorticoids correlated positively with body fat and leptin in men (P < 0.05) but not in women. After adjustment for total adrenal glucocorticoid secretion, net acid excretion was a positive and leptin a negative predictor (P < 0.05) of potentially bioactive free glucocorticoids in women only (total explained variability R2 = 0.71). Our findings indicate that, at least in women, variability of potentially bioactive free glucocorticoids is not only explained by adrenal glucocorticoid secretion but is also metabolically affected by circulating leptin and diet-dependent net acid excretion.

Magnesium and calcium deficiency in humans is related to a number of pathological phenomena such as arrhythmia, osteoporosis, migraine, and fatal myocardial infarction. Clinically established metabolic acidosis induces renal losses of calcium. In normal subjects, even moderate increases in net endogenous acid production (NEAP) impair renal calcium reabsorption but no information is available whether this also influences renal magnesium handling. The aim of the study was to examine the relation between NEAP and renal magnesium excretion in healthy, free-living, elderly subjects. The subjects (age 64 +/- 4.7 y, n = 85) were randomly selected from the population register in Gothenburg (Sweden). Magnesium, calcium, and potassium were measured in 24-h urine samples and NEAP was quantified as renal net acid excretion (NAE). NAE was positively correlated with excretions of magnesium (R(2) = 0.27, P < 0.0001) and calcium (R(2) = 0.30, P < 0.0001) but not potassium. When 24-h urinary magnesium excretion was adjusted for 24-h urinary potassium excretion, a biomarker for dietary potassium intake, the association between magnesium excretion and NAE remained significant (R(2) = 0.21, P < 0.0001). The significant association between potassium-adjusted magnesiuria and NAE suggests that the acid-base status affects renal magnesium losses, irrespectively of magnesium intake. Magnesium deficiency could thus, apart from an insufficient intake, partly be caused by the acid load in the body.

Background: There is increasing evidence that acid-base status has a significant effect on high-intensity physical performance, urolithiasis, and calcium metabolism. Experimental studies in adults showed that renal net acid excretion (NAE) can be reliably estimated from the composition of diets., Objective: We investigated whether a reasonable estimation of NAE is also possible from the dietary records of free-living children and adolescents., Design: Healthy children (aged 8 y; n = 165) and adolescents (aged 16-18 y; n = 73) each collected a 24-h urine sample and completed a weighed diet record on the same day. Urinary NAE was analyzed (NAE(an)) and estimated (NAE(es)). Potential renal acid load (PRAL), the diet-based component of NAE(es), corrects for intestinal absorption of ingested minerals and sulfur-containing protein. A urinary excretion rate of organic acids (OAs) proportional to body surface area was assumed for the complete estimate (NAE(es) = PRAL + OA(es))., Results: Significant (P < 0.001) correlations between NAE(es) and NAE(an) were seen in the children (r = 0.43) and the adolescents (r = 0.51). A simplified estimate based on only 4 components of dietary PRAL (protein, phosphorus, potassium, and magnesium) yielded almost identical associations. Mean simplified NAE(es) (32.6 +/- 13.9 and 58.4 +/- 22.0 mEq/d in the children and the adolescents, respectively) agreed reasonably with NAE(an) (32.4 +/- 15.5 and 52.8 +/- 24.3 mEq/d, respectively)., Conclusions: Predicting NAE from dietary intakes, food tables, and anthropometric data is also applicable during growth and yields appropriate estimates even when self-selected diets are consumed. The PRAL estimate based on only 4 nutrients may allow relatively simple assessment of the acidity of foods and diets.

In early infancy, complex disorders of acid base metabolism are more frequent than in any other age group, with a predisposition to metabolic acidosis due to an age-related low renal capacity for acid excretion and an unphysiologically high actual renal acid load in nutrition with common formulas. Recently in preterm and small-for-gestational-age infants, persistent maximum renal net acid excretion (NAE) with subnormal or normal blood acid base status, impaired weight gain, and adaptive hormonal reactions have been observed. Incipient late metabolic acidosis is one example of a mixed disorder of acid base metabolism with maximum renal NAE in early infancy. Alkali therapy is highly effective and can be realized both on an individual basis, using urine pH screening as a diagnostic criterium for maximum renal acid stimulation, or on a general preventive level using modified standard formula with a reduced actual renal NAE similar to that seen on alimentation with human milk. From an integrated point of view, the low glomerular filtration rate and renal capacity for acid excretion beyond the developmental age of more than 44 weeks, may well be interpreted as the result of a specific adaptation to breast feeding sparing energy, and thus an evolutionary advantage for the survival of mother and child.

To reinvestigate the effect of hCG on circulating and urinary dehydroepiandrosterone sulfate (DHEAS), a hCG stimulation test (5000 IU administered i.m. at 8.30 h on 3 consecutive days) was performed in 6 healthy males (aged 24 to 35 years). Blood specimens and 24-h urine samples were collected immediately before the first and directly after the last hCG administration. Contrary to previous findings in normal men, the present study revealed significant DHEAS responses after testicular stimulation with hCG: plasma DHEAS increased from 7.9 +/- 2.3 to 9.6 +/- 2.2 mumol/L (P < 0.05) and urinary DHEAS from 5.7 +/- 3.6 to 9.3 +/- 5.2 mumol/day (P < 0.05). There was also a marked rise (P < 0.05) in the urinary excretion of total 17-ketosteroid sulfates. Clear increases of unconjugated plasma dehydroepiandrosterone as well as of circulating and renally excreted androstenedione and testosterone definitely confirmed an adequate Leydig cell stimulation. Significant post-hCG changes were additionally observed for plasma and urinary 3 alpha-androstanediol glucuronide (149% and 79% increases, respectively) and for urinary cortisol (21% decrease). Significant correlations were found for the post-hCG percent increases of plasma androstenedione versus plasma DHEAS (r = 0.86) and for the percent increases of plasma testosterone versus urinary DHEAS (r = 0.98), indicating that the extent of gonadal androgen elevations in the circulation of normal men is a determinant of DHEAS increases in blood or urine. These findings provide an explanation for the frequently observed sex differences for DHEAS in adults.(ABSTRACT TRUNCATED AT 250 WORDS)

The object of this study was to determine whether it is possible to reliably estimate the renal net acid excretion (NAE) produced by adults consuming different amounts of dietary protein. A physiologically based calculation model that corrects for intestinal absorption of minerals and sulfur-containing protein and assumes a rate of urinary excretion of organic acids proportional to body surface area was used to estimate NAE. Urinary excretion of different minerals and NAE was measured during the last 48 h of each of four separate 5-d diet periods in six healthy adults. On the basis of food tables, the four nearly isoenergetic diets (one lacto-vegetarian and one high- and two moderate-protein diets) were estimated to yield the following NAE values: 3.7, 117.5, 62.2, and 102.2 mEq/d, respectively. The analytically determined urinary NAE (24.1 +/- 10.7, 135.5 +/- 16.4, 69.7 +/- 21.4, and 112.6 +/- 10.9 mEq/d) corresponded reasonably well to these estimates, suggesting that the calculation model is appropriate to predict the renal NAE from nutrient intake and anthropometric data.

The mineral contents of Na, K, Ca, Mg, Cl and P was determined in different batches of 5 preterm formulas. The purpose of this study was 1st to investigate whether the analytical data are in agreement with the specifications of the manufactures and 2nd whether there are large variations between different batches of the same formula. For each analyzed mineral we found marked differences between the specifications and our measurements in at least one of the formulas. In these cases the differences between the labels and the medians of the analytical data were larger than half of the range of all determinations of the respective formula. Without exception the mean values for K were all clearly lower than the specifications of the producers. In 4 of the 5 premature formulas variation coefficients greater than 10% were observed for at least one mineral. The results show that coincidental variations of mineral contents in different batches can result in a disadvantageous mineral composition because of synergistic effects on metabolism. In this context the importance of the sum of Na and K over Cl in premature formulas is stressed with regard to renal acid excretion. The introduction of more stringent quality standards is proposed.