Renal excretion of calcium and phosphorus in premature infants with incipient late metabolic acidosis.

BACKGROUND: Premature infants receiving alimentation with cow milk-based formulas run a considerably high risk of incipient late metabolic acidosis, an early stage developing of manifest late metabolic acidosis. Is bone metabolism involved in pathophysiologic mechanisms characterizing this early stage of retention acidosis? METHODS: Urinary ionography was performed in 10 premature infants with spontaneous development of incipient late metabolic acidosis (indicated by urine pH < 5.4 on 2 consecutive days) and 10 pair-matched premature infants with normal values of urine pH; both groups were receiving full oral nutrition with the same standard formula. Moreover, in 37 premature infants with incipient late metabolic acidosis who were randomly allocated to oral therapy with 2 mmol. kg(-1). d(-1) of either NaHCO 3 or NaCl over a period of 7 days, urinary excretion of calcium and phosphorus was assessed on day 1 and day 7. RESULTS: Incipient late metabolic acidosis was accompanied by increased phosphaturia in premature infants receiving full oral nutrition. Seventeen premature infants receiving NaCl therapy (19 treatment periods) showed increased calciuria from day 1 to day 7, whereas, in 20 premature infants receiving NaHCO 3 therapy (23 treatment periods), calcium or phosphorus excretion in urine did not increase. CONCLUSIONS: The data of urinary calcium and phosphorus excretion in premature infants support the hypothesis that bone mineralization may already be impaired in the early stage of incipient late metabolic acidosis.

Changes in time-trends of nutrient intake from fortified and non-fortified food in German children and adolescents--15 year results of the DONALD study. Dortmund Nutritional and Anthropometric Longitudinally Designed Study.

BACKGROUND: Although fortified products have played an increasing role in food marketing since the 1980s in Germany, data as to the consumption of fortified food is sparse. AIM OF THE STUDY: To assess long-term data on changes in fortified food supply or consumption patterns, nutrient intake, and time trends in the DONALD Study (Dortmund Nutritional and Anthropometric Longitudinally Designed Study). METHODS: Between 1985 and 2000 consumption of nutrient intake (total and from fortified foods) was evaluated and time trends in energy and nutrient intake were assessed on the basis of 3-day weighed dietary records (n = 4193) of 2-14 year-old males (n = 383) and females (n = 404) enrolled in the DONALD Study. Nutrient intake was expressed as percentage of the current German recommendations. Food products were defined as fortified if enriched with at least one of the following nutrients: Vitamin A or provitamin A carotenoids (summarised as Vitamin A), Vitamins E, B1, B2, B6, C, niacin, folate, calcium or iron. Nutrient supplements and medicine were excluded from this evaluation. Time trends were analysed using linear and non-linear regression models (PROC MIXED, SAS 6.12). RESULTS: In percent of German references [3], non-fortified food contributed to folate intake by 20-30%, to Vitamin E by about 40%, to Vitamin B1 by 50-65%, to Vitamin A, C, B2, calcium, iron by about 65-95%, and to Vitamin B6 and niacin intake by 100% and more. Fortified food alone provided no more than 5% of calcium intake, about 10-20% of iron, Vitamin A and folate intake, up to 40-50% of Vitamin C, B1, B2, E, niacin and up to 80% of Vitamin B6 intake. During the 15 year period of the DONALD Study with total food, we only found a significant linear time trend for Vitamin C, whereas significant non-linear time trends were found for calcium, Vitamin E, B1, B2, B6, niacin and folate. In the latter there was a uniform increase until 1994 and a decrease thereafter. For iron and Vitamin A no significant time trend could be identified. Only iron and Vitamin A intake from fortified food showed a significant linear time trend. All other nutrients studied here gave significant non-linear time trends. Nutrient intake with fortified food reached maximum values between 1994 and 1996 followed by a decrease thereafter. CONCLUSIONS: Signs of changing food consumption patterns were found, pointing to an almost uniform decrease of nutrient intake since 1994/96 in our population of German children and adolescents. This could be an alarming indicator of a slight but unpreferable tendency to eat energydense, nutrient-poor foods.

History of nutrition and acid-base physiology.

In the 17th century the notion of nutrition and diet changed in northern European countries. First chemical experiments fostered the idea that salts resulted from a union of acids and bases. Digestion was no more regarded as a process of cooking but a succession of fermentations controlled by a balanced production of acids and alkali. Life seemed to depend on the equilibrium of acids and alkalis. In the 19th century food was systematically analysed for the content of energy and macronutrients and first scientifically based nutritional standards were formulated. The preferred use of processed food from the new food industry resulted in epidemics of nutritional disorders. Acidosis seemed to be a plausible pathogenic factor. Practitioners (S Ishizuka, H Hay, FX Mayr) formulated holistic doctrines integrating the concept of balance of acids and bases and recommending food with an excess of alkali. New micromethods to determine the concentration of electrolytes and blood acid-base status promoted physiological and clinical research into acid-base metabolism in the 1960s. In the new physiologically based terminology of systemic acid-base status, the relationship between blood acid-base status and net acid intake or excretion was, however, incorrectly simplified. In the 1970s metabolic acidosis was observed in patients on chemically defined diets and parenteral nutrition. Based on the data of comprehensive acid-base balance studies, calculation models were used to estimate renal net acid excretion from nutrient intake and to predict the potential renal acid load of single foods. Extrapolating current trends to the future, one can say that acid-base physiology will probably remain a challenge in nutrition and functional medicine over the next few years. The challenge will include new concepts for the manipulation of nutritional acid load in sports, dietetics and preventive medicine as well as new definitions of the upper intake level of potential renal acid load in functional foods and the monitoring of renal net acid excretion in populations.

Nutrition, acid-base status and growth in early childhood.

Optimal growth is only possible in a well-balanced "inner milieu". Premature infants are especially vulnerable for disturbances of acid-base metabolism with a predisposition to metabolic acidosis due to a transient disproportion between age-related low renal capacity for net acid excretion (NAE) and an unphysiologically high actual renal NAE on nutrition with standard formulas. During a 50 month period, 452 low birth-weight infants were screened for spontaneous development of incipient late metabolic acidosis (ILMA), an early stage during the development of retention acidosis, characterized by maximum renal acid stimulation (MRAS, urine-pH < 5.4) on two consecutive days but still compensated systemic acid-base status. Compared with controls, patients with ILMA showed higher serum creatinine values, an increased urinary excretion of sodium, aldosterone and nitrogen, but only slightly lower blood pH (7.38 vs 7.41) and base excess (-2.8 vs. 0.2 mmol/l) with respiratory compensation (PCO2 35 vs 37 mm Hg). Patients with altogether 149 episodes of ILMA were subsequently randomly allocated to either treatment with NaHCO3 2 mmol/kg/d for 7 days or no special therapy in protocol I, or NaHCO3 vs NaCl each 2 mmol/kg/d for 7 days in protocol II. Patients of protocol I with persistent MRAS for 7 days showed lowest weight gain and a tendency for a further increase in urinary aldosterone and nitrogen excretion. NaCl supplementation (protocol II) seemed to promote weight gain without affecting either impaired mineralization or suboptimal nitrogen retention. Patients with alkali therapy under both protocols showed normal weight gain and normalization of hormonal stimulation, mineralization (protocol II) and nitrogen assimilation. Modification of the mineral content of a standard preterm formula decreased renal NAE to the low level seen on alimentation with human milk and reduced the incidence of ILMA in preterm and small-for-gestational-age infants to 1%. The data show that ILMA is associated with impaired growth. Activation of secondary homeostatic mechanisms (extracellular volume contraction, depletion of disposable net base pools) might be important for impaired growth. Production of new formulas for reduced renal NAE could be an effective general preventive measure to reduce the clinical importance of one component of mixed acid-base disorders in early childhood.

Ten-year trends in vitamin and mineral intake from fortified food in German children and adolescents.

OBJECTIVE: We investigated time trends in consumption patterns, and energy and nutrient intakes (protein, fat, carbohydrates, added sugars, vitamins A, E, C, B1, B2 and B6, niacin, folate, calcium and iron) from fortified food in children and adolescents between 1987 and 1996 in Germany. DESIGN: Mixed longitudinal survey (DONALD study) with 3 d weighed dietary records (n=2062 from 594 subjects), one subject per family per year chosen by random. SETTING: Dortmund (Western Germany) district cohort. SUBJECTS: 285 males, 309 females; mean age 6 y (2-13 y). RESULTS: Almost all children and adolescents consumed fortified food irrespective of the year studied. With the exception of vitamin E, significant time trends in the proportions of nutrient intakes from fortification were observed. The fortification of food with vitamins A, C, B1, B2 and B6 and niacin raised the already adequate intakes from non-fortified food (100% to 150% of reference intake values) by 20-50%. The fortification of food with vitamin E and folate raised the low intakes from non-fortified food (about 50% of reference intake values) to about 80% (folate) and 100% (vitamin E) of the references. Fortification of food with calcium and iron was not significant (<10%), but while total intake of calcium was adequate, total intake of iron remained critical. CONCLUSIONS: Since the nutrient intake of the population of children and adolescents studied is adequate with respect to vitamins A, C, B1, B2 and B6, niacin and calcium, fortification seems inefficient, while fortification of food with vitamin E and folate, but not iron, improves an inadequate intake. SPONSORSHIP: The DONALD study is supported by the German Federal Ministry of Health and the North-Rhine-Westphalian Ministry of Science and Research. European Journal of Clinical Nutrition (2000) 54, 81-86

Vitamin intake of 3- to 36-month-old German infants and children--results of the DONALD-Study.

Infants and young children are a vulnerable group with regard to nutrition. However, there is a lack of information about the dietary composition of healthy German infants and children. Therefore, the intake of vitamins (A, C, E, B1, B2, B6, folate, niacin) was assessed in 354 healthy German infants and children aged 3 to 36 months from 3-day-weighed diet records and compared with German, European and US reference values. Intake of all B-vitamins (B1, B2, B6, folate, niacin) increased during the first 3 years of life, whereas intake of vitamin E decreased. Intake of vitamin A and C varied between age groups. The highest levels of the nutrient densities of most vitamins were found at the end of the first year of life. Depending on the reference values chosen, the vitamin supply of the study population ranged between sufficient and very good. The reported satisfactory intake of vitamins in infants and young children in this study gives rise to the question of whether the current extent of fortification of commercial infant food in Germany is necessary.

Increased risk of iodine deficiency with vegetarian nutrition.

Observational studies primarily based on diet questionnaires or food records have reported that vegetarians can have a very low I intake. However, analytically ascertained data on the possible degree of I deficiency with this form of diet is lacking. Six healthy adult volunteers participated in the present controlled experimental diet study carried out in four separate 5 d diet periods. The study diets, normal, protein-rich, lactovegetarian, and repeat of the initial normal diet, were almost isoenergetic and contained no fish, sea food, iodized salt or processed foods fortified with I. During the last 48 h of each diet period two 24 h urine samples were obtained from each subject. I analyses were performed in the urine samples and in representative samples taken from all ingested diets. Urinary I excretion was significantly lower with the lactovegetarian diet (36.6 (SD 8.8) micrograms/d) than with the normal and the protein-rich diets (50.2 (SD 14.0) and 61.0 (SD 8.0) micrograms/d respectively). Accordingly, a markedly reduced I intake was confirmed analytically for the lactovegetarian diet (15.6 micrograms/d v. 35.2 and 44.5 micrograms/d respectively). Our results provide experimental confirmation of literature findings indicating that I supply is higher with non-vegetarian than with vegetarian diets. Specifically, the extremely low intake and urinary output of I as analytically determined for one exemplary vegetarian diet, demonstrate that dietary I may be limiting when strict forms of vegetarian dietary practices (no iodized salt, no I supplements) are followed. The present study is, therefore, the first diet-experiment-based pointer to the potential danger of I deficiency disorders due to strict forms of vegetarian nutrition, especially when fruits and vegetables grown in soils with low I levels are ingested.

Effect of iodine supply on neonatal thyroid volume and TSH.

A cross-sectional study was performed to prove the correlation between iodine intake and neonatal thyroid volume in a randomized group of 100 mother/newborn pairs. Thyroid volume and iodine excretion were measured by ultrasound and urinary iodine excretion, respectively. Iodine intake and, nutritional and smoking habits were estimated by questionnaire. In 89 mother/child-pairs the data were complete for all parameters and have been analyzed: 32 mothers substituted with iodine tablets, average dose 175 microg K-Iodide/day. Iodine excretion of prenatally iodine-substituted newborns increased by 62% whereas neonatal thyroid volume was reduced by 18% compared with the non-iodine-supplemented group. Smoker's newborns (n = 8) had a thyroid volume 20% larger than that of newborns of non-smokers. Neonatal TSH-screening values remained within normal limits.

Modified cow's milk formula with reduced renal acid load preventing incipient late metabolic acidosis in premature infants.

BACKGROUND: Premature infants receiving alimentation with cow's milk formulas are at a considerably high risk of developing incipient late metabolic acidosis, an early stage in the development of manifest late metabolic acidosis. Is it possible to reduce this risk by modification of the composition of a standard formula? METHODS: The mineral composition of a cow's milk preterm formula A was modified (formula B) with the aim of reducing the alimentary load to that of human milk. 160 premature infants were fed either mother's milk (n = 50) or the modified formula B (enriched with sodium and potassium) (n = 110), and their urine pH was tested twice a week. Randomly collected subgroups of infants were studied in detail for nutrient balances. The results were compared with earlier observations of 282 premature infants fed either mother's milk (n = 28) or the standard formula A (n = 254). RESULTS: Incipient late metabolic acidosis was observed in nine of 78 premature infants receiving mother's milk, 53 of 254 premature infants receiving the standard formula A, and only one of 110 premature infants fed the modified formula B. Net acid excretion was 0.58 mmol/kg/day in 11 premature infants receiving alimentation with the modified formula B compared with 1.73 mmol/kg/day in 23 premature infants fed formula A. This reduction was mainly due to an increased alkali excess (sodium + potassium-chloride) in intake and urine. CONCLUSIONS: Reduction of renal acid load with the modified formula B had a preventive effect on the rate of development of incipient late metabolic acidosis in premature infants.

Body growth in primary de Toni-Debré-Fanconi syndrome.

Body growth in nine children with primary de Toni-Debré-Fanconi syndrome was followed from birth to adolescence or adult life. At the time of diagnosis, corresponding to the start of treatment, the median age was 2.3 (range 0.4-13.9) years and height standard deviation score (SDS) was always decreased (median -3.5, range -6.8 to -2.1). Despite continuous electrolyte and bicarbonate supplementation only four patients showed a slight improvement in growth. At the time of the last observation at the age of 17.2 (4.5-20.1) years median height was -4.7 (-5.9 to -1.8) SDS. The median difference between height at last observation and target height was -4.5 SDS. Final height (n = 5) ranged between -1.8 and -5.5 (median -4.3) SDS. The pubertal growth spurt was absent in two children. Metabolic acidosis was identified as a significant growth-retarding factor. Mean serial blood bicarbonate levels and height SDS at the last observation were correlated (r = -0.87, P < 0.01). No correlation was observed between last height SDS and the degree of hypokalemia, hypophosphatemia, or hypercalciuria. In conclusion, patients with primary de Toni-Debré-Fanconi-syndrome present severe growth failure at the time of diagnosis which persists into adult life. Supportive therapy is frequently unable to prevent further loss of relative height.

The short-term effect of dietary pectin on plasma levels and renal excretion of dehydroepiandrosterone sulfate.

Studies specifically investigating the effects of single dietary components on plasma levels of dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) are rare. Especially no data is available with regard to specific dietary fibers. Therefore, the impact of pectin (a representative fiber that affects the enterohepatic recirculation of bile acids) was studied in a randomized crossover trial consisting of three diet periods characterized by the same food supply and daily doses of 0 g, 15 g or 30 g pectin. Blood and 24-h-urine samples were collected at the end of each 4-day diet period from 6 healthy male volunteers. Plasma levels of DHEA, cortisol and the major binding protein of DHEAS albumin remained unchanged with the varying pectin supplements. Also, no changes were observed for several urinary analytes including urinary DHEAS. However, effects of pectin intake (30, 15 versus 0 g/d) were seen for plasma DHEAS (9.3 +/- 2.8, 9.2 +/- 2.6, 8.0 +/- 3.1 mumol/L, p < 0.01) and total plasma cholesterol (4.4 +/- 0.7, 4.5 +/- 0.7, 4.7 +/- 0.8 mmol/L, p = 0.1). Obviously, the altered intake of fiber in the form of pectin affects plasma concentrations of DHEAS and cholesterol in an opposite direction. The reason for this is not known but a dietetically induced modulation of the binding properties of plasma albumin for DHEAS appears possible. Our findings suggest that the target tissue-available, not protein-bound fraction of circulating DHEAS (as reflected by the renal DHEAS output) is not necessarily altered when total plasma concentrations of DHEAS vary.

[Supplementation of premature infant nutrition with calcium and phosphor for improving mineral supply of premature and small-for-gestational age newborn infants]. / Anreicherung einer Frühgeborenenmilchnahrung mit Kalzium und Phosphor zur Verbesserung der Mineralstoffversorgung Früh- und Mangelgeborener.

A standard preterm formula was supplemented with calcium (Ca) and phosphorus (P) (F-CaP: Ca 87 mg/dl, P 43 mg/dl) and compared to the non-supplemented form (F: Ca 62 mg/dl, P 36 mg/dl). VLBW and small-for-gestational-age infants (n = 79) were included in the study which was performed to look for adverse effects and to decide about a reasonable start and duration of supplementation. In preterm infants with a birth weight lower than 1500 g and a body weight of more than 2000 g, the additional supplementation with Ca and P lead to a significant higher Ca- and P-retention without further load for the kidney. In addition, preterm infants with a body weight lower than 1500 g also had a better retention of Ca and P. Both, F-CaP and F lead to a high urinary excretion of phosphorus, a high renal net acid excretion and a relatively high activity of serum alkaline phosphatase. Anthropometric measurements did not reveal any evidence for an impaired caloric absorption due to an increased fecal fat excretion. Hypercalcemia or hyperphosphatermia was not seen. Hypercalciuria occurred in less than 5% of the samples studied. The results of this study indicate that a continuation of the supplementation with Ca and P is justified in VLBW infants with a body weight of more than 2000 g. There was no evidence for adverse effects of Ca and P supplementation in VLBW infants with a body weight lower than 1500 g, who might therefore also benefit from supplementation. Further studies are necessary to investigate unsatisfactory metabolic conditions of these children e.g. the high renal load.

Increased renal net acid excretion in prematures below 1,600 g body weight compared with prematures and small-for-date newborns above 2,100 g on alimentation with a commercial preterm formula.

In 76 low birth weight infants with an actual body weight ranging from 1,210 to 2,540 g and fed a commercial preterm formula, urine samples were collected and blood acid base status was measured on day 38 (+/- 17, mean +/- SD) of life. Infants with an actual body weight below 1,600 g demonstrated a higher daily weight gain (22 +/- 3 vs. 14 +/- 5 g/kg/day), lower blood pCO2 (35.4 +/- 5.0 vs. 38.9 +/- 3.8 mm Hg), lower urine pH (5.8 +/- 0.5 vs. 6.5 +/- 0.3), higher renal net acid (1.86 +/- 0.38 vs. 1.28 +/- 0.55 mmol/kg/day) and higher phosphorus excretion (0.67 vs. 0.52 mmol/kg/day) than infants with an actual body weight above 2,100 g. Urinary ionogram data of these 2 groups of infants show that the increased renal net acid excretion of the smaller prematures is the result of a lower urinary excretion of sodium, potassium and chloride, due to a higher daily weight gain, probably a higher retention of these minerals, and a higher urinary phosphorus excretion probably due to an age-specific lower intestinal calcium absorption, and therefore a lower rate of calcium and phosphorus retention. Considering the low renal capacity for hydrogen ion excretion, very low birth weight infants still run a considerable risk for disturbances of acid base metabolism due to the high mean level of net acid excretion in nutrition with preterm formulas and an additional age-specific augmentation of renal acid load.

[Nutritional iodine status of healthy infants in Germany]. / Jodversorgungszustand gesunder Säuglinge in Deutschland.

In 78 healthy term babies from Düsseldorf and surroundings spontaneous urine samples were collected on day 108 to day 144 of life and analyzed for the content of iodine and creatinine. 26 babies were breast fed. 23 babies received an iodized hypoallergenic formula and 26 babies different commercial formulas only partly iodized. From 4 parameters to estimate iodine supply of the babies (urinary iodine concentration microgram/dl, iodine/creatinine ratio microgram/g; estimated daily iodine excretion microgram/d, estimated daily iodine excretion corrected for body surface area microgram/dl 1.73 m2) estimated daily iodine excretion was the most useful parameter. Breast fed babies showed a significantly lower estimated daily iodine excretion (median 32 microgram/d) than babies fed the hypoallergenic (52 microgram/d) or a commercial formula (54 micrograms/d). In Germany with an insufficient iodine supply of pregnant and lactating mothers breast fed infants run a risk for an insufficient iodine supply. Furthermore, supplementation of infant formulas with iodine started in 1990/1991 proved to be a sufficient measure to correct iodine deficiency.

Low renal net acid excretion, high calciuria and biochemical signs of sodium deficiency in low-birth-weight infants fed a new low-phosphorus formula.

In 11 infants (birth weight greater than 1800 g) fed a new type of humanized formula with a low phosphorus (P) content (calcium (Ca) 11 mmol/l, P 7.2 mmol/l, sodium (Na) 8.3 mmol/l) biochemical parameters of blood, serum and urine were determined. In nine boys Ca and P balances were evaluated also. Renal net acid excretion was low (0.85 mmol/kg/day). Mean concentrations of P and Ca in urine were 0.34 mmol/kg/day (10.5 mg/kg/day) and 0.1 mmol/kg/day (4 mg/kg/day), respectively. In four infants, Ca concentration in urine was, however, greater than 0.15 mmol/kg/day) (6 mg/kg/day). In infants with birth weights greater than 1800 g fed the new, low-P formula, the low renal net acid excretion, the normal P and the high Ca concentrations in urine were comparable to term infants fed human milk. The high calciuria in several infants may be normal physiologic values. However, it remains to be established that the urinary solubility product of infants fed the new, low-P formula is in the same range as those for infants fed human milk. Unexpectedly, low urinary Na excretion (0.26 mmol/kg/day) and increased urinary excretion of aldosterone-18-glucuronide indicated biochemical evidence of Na deficiency secondary to low Na intake and a high weight gain. If the new, low-P formula is to be fed to infants with a birth weight as low as 1800 g. Na content should be higher than in mature human milk because of the often relatively higher weight gain.

Why is the phosphorus content of human milk exceptionally low?

The phosphorus supply of children and adults is adequate, and usually in excess. Therefore, it is surprising that in breast-fed infants phosphorus intake is very low. This is very rare among mammals. In infants three pathophysiological mechanisms argue in favour of a low, but adequate phosphorus intake in the presence of a balanced ratio of calcium to phosphorus. A low intestinal phosphorus concentration is an essential condition of an acid pH of the faeces, inhibiting the growth of potentially pathogenic germs. Owing to the characteristic renal physiology of the newborn, a small metabolic phosphorus surplus results in a high serum phosphorus level, a well-known risk factor for several disorders, e.g. hypocalcaemic tetany. During infections, impairment of intestinal calcium but not of phosphorus absorption results in an increased phosphorus and renal net acid excretion. Considering the low renal capacity for acid excretion in newborns, a high intake of calcium and phosphorus is a risk factor for the development of metabolic acidosis. It is thought that all three pathophysiologic mechanisms were effective in the biochemical evolution of humans, selecting women with a low phosphorus milk and infants with a constant high intestinal absorption rate of phosphorus.

Glycero- vs glucose-phosphate in parenteral nutrition of premature infants: a comparative in vitro evaluation of calcium/phosphorus compatibility.

In total parenteral nutrition (TPN) of premature infants, glycero- and glucose-phosphate have been recommended, and clinically used, because of their considerable compatibility with calcium. However, a systematic comparative in vitro assessment of the therapeutic potential and safety of these substances has not yet been provided. We investigated the stability of TPN solutions containing calcium-gluconate and glycero- or glucose-phosphate in high concentrations. Evaluation was performed by visual inspection, absorptiometry, light microscopy, measurement of pH, and determination of calcium concentration before and after microfiltration. Even under circumstances promoting precipitation of calcium and phosphate--such as body temperature, relatively high pH, and concentrations of calcium and phosphorus exceeding those necessary to provide intrauterine accretion rates, all but one of the examined TPN admixtures remained stable. Our data suggest that the use of glycero-phosphate, and particularly glucose-phosphate, together with calcium-gluconate, is an uncomplicated and safe procedure to administer simultaneously high amounts of calcium and phosphorus in TPN of premature infants.

Suboptimal mineral composition of cow's milk formulas: a risk factor for the development of late metabolic acidosis.

Late metabolic acidosis was observed in a term baby boy with renal tubular acidosis type 4 who received two cow's milk formulas in succession. Suboptimal mineral composition of the formulas turned out to be an important risk factor for the development of late metabolic acidosis.

Biochemical evidence for the need of long-term mineral supplementation in an extremely low birth weight infant fed own mother's milk exclusively during the first 6 months of life.

In an extremely low birth weight infant fed expressed own mother's milk exclusively during the first 6 months of life, introduction of a human milk fortifier resulted in improvement of biochemical alterations consistent with metabolic bone disease of prematurity. Attempts to discontinue fortification at 9 weeks (discharge) and 21 weeks of age induced deterioration of biochemical parameters, demonstrating a persistent need for mineral supplementation during the whole period of breast-feeding. The effects of long-term human milk fortification are discussed.

Effect of calcium supplementation on calcium and phosphorus balance and renal net acid excretion in preterm infants fed a standard formula.

In 19 preterm infants fed a standard formula for prematures (calcium (Ca) 13.5 mmol/l; phosphorus (P) 12.9 mmol/l), biochemical parameters of blood, serum and urine were determined before and during supplementation with Ca-L-lactate (final Ca concentration 20 mmol/l). In 8 preterm boys Ca and P balance were evaluated in addition. During Ca supplementation, the serum Ca levels, urine pH (without supplement 6.31, with supplement 6.73), and calciuria (46 mumol/kg/d vs. 98 mumol/kg/d) were increased, and urinary P (1.05 mmol/kg/d vs. 0.65 mmol/kg/d) and net acid excretion (1.70 mEq/kg/d vs. 0.89 mEq/kg/d) were decreased. Balance studies showed increased net intestinal Ca absorption during supplementation (37% vs. 56%) as well as improved Ca (0.8 mmol/kg/d vs. 1.85 mmol/kg/d) and P retention (0.97 mmol/kg/d vs. 1.45 mmol/kg/d). These data show that increased Ca intake given to optimize the Ca:P ratio improves mineral retention in preterm infants fed a standard formula. Ca and P intake should be thoroughly balanced to avoid side-effects like hypercalciuria or high renal net acid excretion.