Urinary antimony in infancy

Accepted 6 January 1997
OBJECTIVE—To determine whether antimony may be detected in the urine during infancy and early childhood and its association with passive exposure to tobacco smoke, as assessed by urinary cotinine.
DESIGN—Analysis of spare aliquots of urine collected from infants participating in studies of respiratory function and passive smoking. Urinary antimony was assayed using inductively coupled plasma mass spectroscopy in 201 urine specimens collected at different ages throughout the first two years of life from 122 term and 26 preterm infants. Urinary cotinine was measured using gas liquid chromatography.
MAIN OUTCOME MEASURE—Urinary antimony concentrations.
RESULTS—Absolute antimony concentrations varied widely between infants, being below the laboratory detection limit of 0.02 µg/l in 7% of samples, below 0.5 µg/l in 90.5%, and above the reference value of 1 µg/l reported for non-occupationally exposed UK populations in 4%. Creatinine standardised antimony values were unrelated to postnatal age or urinary cotinine concentrations and were highest in urine collected from preterm infants within 24 hours of birth (geometric mean (95% confidence interval): 2.3 ng/mg (1.5 to 3.4)).
CONCLUSION—Although antimony is present at very low concentrations in urine during infancy and early childhood, the relevance to health is uncertain. The higher levels found in preterm infants may reflect prematurity or fetal assimilation of antimony. Tobacco is unlikely to be an important source of environmental exposure to antimony during infancy and early childhood.

     

Urinary S-100B concentrations in term and preterm infants at risk for brain damage

BACKGROUND: Elevated serum concentrations of S-100B, a 21-kDa protein expressed in astroglial cells, has been used to assess cerebral damage after head trauma, infection, ischemia, and perinatal asphyxia. OBJECTIVE: As S-100B is eliminated by the kidneys, we investigated the feasibility of measuring S-100B in urine of newborns with severe perinatal asphyxia, and in very low birth weight (VLBW) preterm infants at risk for neurodevelopmental impairment. METHODS: We first analyzed urine samples of 8 term or near-term newborns without major medical problems, followed by urine samples of 2 term newborns with severe birth asphyxia, and finally urine samples of 8 VLBW (gestational age 24-28 weeks) infants collected every 4 h for up to 10 days. RESULTS: Urinary S-100B concentrations in 8 term or near-term newborns without major medical problems were consistently <1 microg/l. In 2 term newborns with severe asphyxia (Apgar 0/0/0 and 0/2/4) who subsequently had widespread cerebral damage on magnetic resonance imaging, peak urinary S-100B concentrations on the first day of life were 28.1 and 28.4 microg/l, respectively. In 5/8 VLBW infants, urinary S-100B was> microg/l in samples obtained on the first day of life (range 1.2-44.9 microg/l, median 6.8 microg/l). Peak S-100B in urine samples collected during the first 12 h of life were negatively related to gestational age (R(s)=-0.882, p=0.009). Three of the 8 preterm infants had peak urinary concentrations>0 microg/l but neither ultrasound signs of brain damage nor neurodevelopmental delay at 1 year corrected age. CONCLUSIONS: The determination of urinary S-100B concentrations might be helpful in term infants with severe asphyxia, while high urinary S-100B concentrations in preterm infants are to be attributed to immaturity.     

Perinatal bile acid metabolism: analysis of urinary unsaturated ketonic bile acids in preterm and full-term infants

AIM: To compare urinary concentrations of unsaturated ketonic bile acids in preterm and full-term infants. METHODS: Urinary unsaturated ketonic bile acids were determined using gas chromatography-mass spectrometry. RESULTS: Urinary concentrations of total bile acids in early preterm infants (of less than 29wk gestational age) exceeded concentrations in late preterm (between 30 and 37 wk) and full-term infants (between 38 and 41 wk; p < 0.01). The percentage of ketonic bile acids (7alpha, 12alpha-dihydroxy-3-oxo-4-cholenoic acid and 7alpha-hydroxy-3-oxo-4-cholenoic acid) among total urinary bile acids in full-term infants (20.2 +/- 14.1%) was higher than that in early preterm infants (8.94 +/- 8.1%; p < 0.05). The percentage of unsaturated bile acids (3beta-hydroxy-delta5-bile acids) among total bile acids in urine did not differ greatly between groups. CONCLUSION: The percentage of 3-oxo-delta4 bile acids among total bile acids in urine gradually increased from early to late preterm infants, while healthy full-term infants excreted large amounts of 3-oxo-delta4 bile acids in urine at delivery.     

Cigarette smoke exposure and development of infants throughout the first year of life: influence of passive smoking and nursing on cotinine levels in breast milk and infant''s urine

The effects of smoke exposure via mothers' milk and/or via passive smoking during the first year of life were investigated in a prospective longitudinal matched-pair study. The somatic and mental development of 69 infants whose mothers smoked more than five cigarettes per day throughout pregnancy and continued smoking after childbirth were compared with 69 children of non-smoking mothers. At birth, mean body weight of neonates from smoking mothers was significantly lower than the weight of neonates from non-smoking mothers. This weight difference between the two groups was no longer significant in infants at 12 months of age. With the methods employed by the authors, neither psychomotor nor mental development was affected by smoke exposure during pregnancy and early infancy. Infections of the lower respiratory tract were more frequent in the children of smoking mothers. These mothers weaned their babies earlier than non-smokers, but the different feeding behaviour did not influence any of the clinical parameters that were investigated in this study. In order to evaluate the extent of smoke exposure, cotinine was measured in children's urine and in breast milk once a month throughout the first year of life. Cotinine in the urine was significantly dependent on feeding behaviour: infants breast fed showed concentrations 10-fold higher than those who were bottle fed. Cotinine excretion in urine of infants from smoking mothers, who were not breast fed (nicotine exposure via passive smoking only) was even higher than that of adult passive smokers. If infants from smoking mothers were breast fed, their urinary cotinine excretion was in the range of adult smokers.(ABSTRACT TRUNCATED AT 250 WORDS)     

Calcium and phosphor intake in preterm infants: sensitivity and specifity of 6-hour urine samples to detect deficiency

Aim of the present study was to test whether six-hour (6 h) urine specimens predict the 24-hour (24 h) mineral homeostasis in individual infants born preterm. Urinary Calcium (Ca) and Phosphate (P) concentrations were studied in 60 stable infants; gestational age 34 (25-42) weeks. In 58 infants four 6 h urine specimens and in 2 infants all spot urine specimens obtained within 24 h were analyzed. In 39 infants born preterm coefficients of variation were 0.42 (SD 0.26) and 0.41 (SD 0.26) for Ca and P measurements in the four 6 h urine specimens obtained within 24 h, respectively, The mineral homeostasis of the infants was defined as Ca or P surplus homeostasis if the 24 h urinary concentrations were ≥1 mmol/l. The sensitivity, specificity, and PPV of a 6 h urinary specimen to predict Ca deficiency homeostasis (24 h urinary Ca <1 mmol/l) were 0.93 (0.77-0.98; 95%CI), 0.72 (0.43-0.90) and 0.90 (0.74-0.96). The sensitivity, specificity and PPV for urinary P were 0.8 (0.38-0.96), 0.97 (0.85-0.995), and 0.8 (0.38-0.96). In conclusion, in infants born preterm on regular 3 or 4 h feedings, 6 h urine sampling is sufficiently precise for prediction of Ca and P mineral deficiency homeostasis (PPV 0.92 and 0.83). However, measurements at regular intervals (twice weekly) are recommended not to miss any infant in mineral deficiency homeostasis.     

Urinary excretion of epidermal growth factor in the newborn

Urinary epidermal growth factor (EGF) excretion was studied serially in 36 newborn infants, from 26 to 40 weeks gestation, from birth to three months of age. All infants excreted EGF from birth. Excretion was significantly higher in term infants than in preterm infants at birth; in term infants excretion rose steadily in early infancy and there was a similar but delayed rise in EGF excretion by preterm infants. Urinary EGF excretion appears to be related to age from conception and birth does not influence it. There was no correlation between urinary EGF excretion and the rapid maturation of the lungs and skin which occurs in preterm infants in the early neonatal period.     

Study of passive smoking measured by urinary cotinine in maternal and child protective health centers in North-Pas-de-Calais]

BACKGROUND: The aim of the study was to determine the circumstances of exposure to environmental tobacco smoke, to evaluate its importance by measurement of urinary cotinine, and to study the relationship with the children's medical history. POPULATION AND METHODS: It was a prospective investigation realized in 20 outpatient pediatric clinics. The parents answered a questionnaire to assess the child's exposure as well as the child's medical and surgical history. Cotinine was measured in urine samples collected during the visit. Concentrations > 6 ng/mL were considered to be positive. RESULTS: Two hundred and one children were included in the study (mean age 17 months, extremes: 1-72 months), 107 of whom were exposed to environmental tobacco smoke. Urinary cotinine was found to be positive in 27 cases (13%). There was a positive relation between passive tobacco exposure and positive urinary cotinine (P < 0.001). Eighty of 201 mothers and 135 of 185 fathers smoked. There was a relation between positive urinary cotinine and the mother's smoking, as well as with a history of upper respiratory tract infection (rhinitis, otitis media) or adenoidectomy. No relation was found between a history of bronchiolitis and passive smoking. CONCLUSIONS: Passive tobacco exposure is very frequently encountered in our region. Urinary cotinine, which can be easily measured, might constitute an efficient tool in order to convince the parents of the reality of passive smoking.     

Urinary lithogenic and inhibitory factors in preterm neonates receiving either total parenteral nutrition or milk formula

The aim of this study was to evaluate prospectively the influence of nutrition on certain factors which may inhibit or promote nephrocalcinosis in two groups of preterm infants, receiving total parenteral nutrition (TPN) and special preterm milk formula respectively, but not furosemide. A total of 37 preterm infants, 15 on TPN and 22 fed a special preterm formula were studied at the end of the 1st, 2nd and 3rd weeks of life, at which time serum and 8 h urine specimens were collected. High ratios of urinary calcium to urinary creatinine (UCa/cr), urinary oxalate to urinary creatinine (Uox/cr) and urinary calcium to urinary citrate (UCa/cit) indicates an increased risk for nephrocalcinosis while high urinary citrate to urinary creatinine (Ucit/cr) ratio indicates protection. Uox/cr increased significantly (P<0.05) in those infants fed preterm formula, from the end of 2nd week of life and was two-fold higher than in the TPN group of preterm infants (P<0.01). Ucit/cr was higher throughout the study period in the formula fed than in the TPN preterm infants. UCa/cit was five-fold higher (P<0.01) in the TPN group, by the end of the 3rd week. Urinary calcium and magnesium was similar in both groups during the study period. Two of the infants studied (5.4%), one from each group, developed nephrocalcinosis.CONCLUSION: In preterm neonates on total parenteral nutrition, urinary oxalate -to-creatinine ratio (a potent lithogenic factor) was lower and urinary citrate -to-creatinine ratio (a lithoprotective factor) also lower than in formula fed neonates. The type of feeding (total parenteral nutrition or special preterm milk formula) seems to affect urinary oxalate and citrate but not calcium and magnesium in non-furosemide treated preterm infants during the first 3 weeks of life.     

Postnatal urinary conductance measurement in preterm infants

The aim of this study was to determine whether serial urinary conductance measurements can be used to estimate reliably the end of the transition period of negative sodium balance in preterm infants. The relationship between urine conductance, measured by a conductance meter, and urine sodium concentration was determined in 109 pooled samples of urine obtained from 14 preterm infants during the transitional period of fluid balance. It was shown by linear regression analysis that urine sodium concentration (mmol l -1 ) = 0.78 ×urine conductance -1.25. Urine sodium concentrations derived from the above formula were concordant with urine sodium measured directly when used to calculate daily sodium balance in all 14 infants.

Conclusion: Urine conductance can be accurately measured at the cotside by neonatal nurses and used to identify the timing of the postnatal transition from negative to positive sodium balance in preterm infants. These findings can help in making decisions on the introduction of postnatal sodium administration to preterm infants.     

Fetal bile acid metabolism: analysis of urinary 3beta-monohydroxy-delta(5) bile acid in preterm infants

To elucidate the urinary concentration of total bile acids after birth and the profile of the usual and unusual urinary bile acids, especially 3beta-hydroxy-5-cholen-24-oic acid (Delta(5)-3beta-ol), we measured the concentrations of 13 bile acids in the urine from preterm infants vs. full-term controls by gas chromatography-mass spectrometry. The urinary concentration of total bile acids in early preterm infants below 32 weeks of gestational age significantly exceeded that of the late preterm and full-term infants (p < 0.0005). The major urinary bile acids in early preterm infants were cholic acid, 1beta,3alpha,7alpha,12alpha-tetrahydroxy-5beta-cholan-24-oic acid and Delta(5)-3beta-ol. In conclusion, the high urinary concentrations of total bile acids in preterm infants may be due to an overproduction, or more likely to a low hepatic bile acid clearance. An alternative fetal pathway, the acidic pathway, may be a major route of bile acid biosynthesis in preterm infants.     

Nicotine and cotinine concentrations in serum and urine of infants exposed via passive smoking or milk from smoking mothers

The exposure of infants to nicotine via milk of smoking mothers or via inhaled side-stream smoke ("passive smoking") was evaluated. Newborn infants nursed by smoking mothers and unexposed to passive smoking showed measurable serum concentrations of nicotine (0.2 to 1.6 ng/ml) and its main metabolite, cotinine (5 to 30 ng/ml), and also excreted measurable amounts of nicotine and cotinine in their urine: the ratio of nanograms of nicotine/milligrams of creatinine (N/C ratio) ranged from 5.0 to 110 (median 14), and the corresponding ratio of nanograms of cotinine/milligrams of creatinine (C/C ratio) from 10 to 555 (median 110). Infants of the same age nursed by nonsmoking mothers did not excrete measurable amounts of the two substances except in one case. Older and non-breast-fed infants exposed only to passive smoking had N/C ratios in the range of 4.7 to 218 (median 35) and C/C ratios in the range of 117 to 780 (median 327 ng/mg). Infants exposed to passive smoking and to smoke via breast milk had N/C ratios in the range of 3.0 to 42 (median 12) and C/C ratios in the range of 225 to 870 (median 550). The significant serum concentrations and urinary excretion rates of nicotine in the breast-fed infants of smoking mothers suggest that nursing contributes to the nicotine exposure of these neonates. In older infants, the wide variation of cotinine excretion values did not allow separate evaluation of the two exposure routes.     

Nicotine exposure in breastfed infants

AIM: To study exposure to nicotine in breastfed infants in relation to parental smoking habits. MATERIAL AND METHODS: Forty mother-infant pairs were studied. Twenty non-smoking mothers, 18 smoking (2-20 cigarettes per day) and two snuff-taking mothers were included. All infants were healthy, exclusively breastfed and their postnatal age was 6 wk. During a home visit, parental smoking habits were recorded, and the time of mothers' last smoke or taking of snuff and breastfeeding were recorded. Breast milk and infant urine samples were collected. Concentrations of nicotine and cotinine were analysed with gas chromatography. The amount of milk ingested during the home visit was calculated by weighing the infants. RESULTS: Two non-smoking and non-snuff-taking women had milk containing nicotine (28 and 13 microg/l, respectively). Both had smoking spouses. In the smoking and snuff-taking group, the mean (SD) milk nicotine concentration was 44 (38) microg/l (n = 36). When milk samples taken 7 h and 0.6 h after smoking were compared, the concentration of milk nicotine increased from 21 to 51 microg/l (p < 0.01). The two snuff-taking mothers exposed their children to higher milk nicotine concentrations than all but two of the smokers. The concentrations of the metabolite cotinine in infant urine correlated with the dose of nicotine ingested during the home visit (r = 0.84, p < 0.01). CONCLUSIONS: Breastfed infants with a smoking or snuff-taking mother are exposed to nicotine in breast milk. The mean intake of nicotine via milk is 7 microg/kg/d. With a shorter time between the mothers' smoking and breastfeeding, the milk nicotine concentration will increase. Both passive smoking at home and snuff-taking were associated with measurable nicotine levels in milk. Healthcare personnel promoting breastfeeding should be aware of these factors influencing exposure to nicotine in the breastfed infant.     

Calcium, sodium and potassium urinary excretion during the first five days of life in very preterm infants

BACKGROUND: Hypercalciuria has been associated with the risk of nephrocalcinosis and renal stones in both adults and children. Renal calcifications are frequently encountered in preterm infants because this particular population presents most of the risk factors of increased urinary calcium excretion. Urinary calcium excretion has been shown to correlate with sodium and potassium excretions in adult patients, but these correlations have not been demonstrated in the early neonatal period yet. OBJECTIVE: To define the relationship between calcium urinary excretion and sodium or potassium excretions in the first 5 days of life in preterm babies. METHODS: A prospective study was conducted in 16 preterm infants born before 32 weeks of gestation (body weight 1,373 +/- 310 g; gestational age 29.1 +/- 1.6 weeks). Fifteen consecutive 8-hour urine collections were performed for each infant from the 8th hour of life. A plasma sample was obtained at the end of each urine collection. Sodium, potassium, calcium and creatinine were measured in urine and blood samples as often as possible. RESULTS: (1) Urine sodium excretion was 6.56 +/- 4.35 mmol/kg per day. (2) Urinary calcium excretion was 5.9 +/- 5.4 mg/kg per day and the urinary calcium/creatinine ratio was 0.48 +/- 0.39 mg/mg. (3) Urinary calcium and sodium excretion were positively correlated (r = 0.65, p = 0.0001), while an inverse correlation was found between calcium and potassium excretion (r = 0.31, p = 0.004). CONCLUSION: The mean values of urinary calcium excretion and calcium/creatinine ratio observed in our population were higher than 4 mg/kg per day and 0.4 mg/mg, respectively, i.e. boundary values previously associated with an increased risk of nephrocalcinosis. We hypothesize that an increase in urinary sodium excretion in this population may facilitate calcium excretion.     

Breast-feeding and environmental tobacco smoke exposure.

BACKGROUND: Exposure to environmental tobacco smoke is associated with adverse effects in infants and children. OBJECTIVE: To explore whether an increase in urinary cotinine fumarate level is caused by ingested nicotine and cotinine in breast-feeding infants. METHODS: We studied newborns at risk for developing asthma and allergies based on a strong family history. We measured urinary cotinine levels in the infants as a measure of environmental tobacco smoke exposure and cotinine levels in the breast milk of breast-feeding mothers. RESULTS: Of 507 infants, urinary cotinine levels during the first 2 weeks of life were significantly increased in infants whose mothers smoked. Breast-fed infants had higher cotinine levels than non-breast-fed infants, but this was statistically significant (P<.05) only if mothers smoked. Urinary cotinine levels were 5 times higher in breast-fed infants whose mothers smoked than in those whose mothers smoked but did not breast-feed. CONCLUSIONS: Mothers should be encouraged to not smoke, and parents must be advised of the potential respiratory and systemic risks of environmental tobacco smoke exposure to their child, including the potential for future addiction to smoking.     

Effect of human breast milk on biological metabolism in infants

The metabolic changes that occur during the postnatal weaning period appear to be particularly important for future health, and human breast milk is considered to provide the optimal source of nutrition for infants. Our previous studies examined the effect of feeding type on antioxidative properties, glucose and insulin metabolism, the lipid profile, metabolomics, and prostaglandin (PG) metabolism in term and preterm infants. A urinary marker of oxidative DNA damage (8‐hydroxy‐2′‐deoxyguanosine) was significantly lower in breast‐fed term and preterm infants than in formula‐fed infants. Markers of insulin sensitivity were significantly lower and atherosclerotic indices were significantly higher in breast‐fed preterm infants than in mixed‐fed infants at discharge. On urinary metabolomics analysis, choline, choline metabolites, and lactic acid were significantly lower in breast‐fed term infants than in formula‐fed infants. Urinary PGD₂ metabolite level in breast‐fed term infants was also significantly lower than in formula‐fed term infants. This indicates that human breast milk affects biological metabolism in early infancy.     

Developmental pattern of urinary bile acid profile in preterm infants

Background:  Bile acid metabolism in preterm infants is yet to be fully characterized. We compared the developmental pattern of urinary bile acid profiles in ten infants born at gestational ages from 25 to 33 weeks with previous data from full-term infants from birth to about 7 months of age.
Methods:  Gas chromatography–mass spectrometry was performed on serial samples.
Results:  Total urinary bile acid concentrations gradually increased until 1 to 2 months of age. After this peak of excretion (30 to 60 µmol/mmol creatinine), total urinary bile acid concentrations gradually decreased to less than 20 µmol/mmol creatinine. The percentage of usual bile acids (mainly cholic acid) relative to total urinary total bile acids gradually deceased from approximately 30% at birth to less than 15% at 7 months of age. On the other hand, 1β-hydroxylated bile acids (mainly 1β,3α,7α,12α-tetrahydroxy-5β-cholan-24-oic acid) relative to total urinary bile acids were increased gradually from 60% at birth to reach 70% to 80% at 1 month of age. The percentage of 1β-hydroxylated bile acids relative to total urinary bile acids then remained stable at a high percentage (70% to 90%) until the age of 7 months.
Conclusion:  Physiological cholestasis in preterm infants persists longer than in full-term infants. Moreover, as large amounts of cholic and 1β,3α,7α,12α-tetrahydroxy-5β-cholan-24-oic acids were detected in urine from preterm infants during this study, the 25-hydroxylation pathway may be particularly important for bile acid synthesis in early preterm infants.     

Renal injury in sick newborn infants: a prospective evaluation using urinary beta 2-microglobulin concentrations

Urinary concentrations of beta 2-microglobulin and creatinine were measured serially in 140 sick infants, of whom 109 were asphyxiated, and in 35 healthy preterm and term infants. First voided urines and samples from days 3 and 7 postpartum were studied. Urinary beta 2-microglobulin concentrations in healthy infants averaged 1.34 +/- 1.34 mg/L (mean +/- SD) in first voided specimens and 1.32 +/- 0.98 mg/L in day 3 samples; the calculated upper limit of normal (95% confidence limit) was 4.00 mg/L. Elevated values (those exceeding the 95% confidence limit) occurred most often in the sick asphyxiated patients (56%); the first voided sample value in these patients was 10.0 +/- 10.4 mg/L. The equivalent value in the sick nonasphyxiated infants was 8.32 +/- 7.27 mg/L. Values were significantly and persistently elevated in the sick infants on days 3 and 7. Factoring beta 2-microglobulin levels by urinary creatinine concentration did not affect the significance of the findings. The increased urinary beta 2-microglobulin levels were not (1) related to gestational age; low beta 2-microglobulin values occurred at all gestational ages for both healthy and sick infants; (2) a consequence of urine flow rate; urinary beta 2-microglobulin did not correlate with urinary creatinine concentration or with urine to plasma creatinine ratio; and (3) a consequence of increased production of beta 2-microglobulin; urinary and serum beta 2-microglobulin values did not correlate (r = .03). Thus, we propose that the elevated levels of urinary beta 2-microglobulin in the sick infants were the consequence of tubular injury. This was associated with hematuria but not with a high incidence of azotemia or oliguria.(ABSTRACT TRUNCATED AT 250 WORDS)     

Normal values for urinary N-acetyl-beta-glucosaminidase excretion in preterm and term babies.

Urinary N-acetyl-beta-glucosaminidase (NAG) excretion was measured in 14 healthy, preterm, male neonates with gestational ages between 32 and 35 weeks. Daily NAG excretion increased significantly during the first four weeks of life. No correlation was observed between urinary NAG:creatinine ratio and postnatal age regardless of whether measurements were taken from the whole 24 hour urine collection or from an isolated urine spot sample at the same time on each day. When the preterm infants were compared with a group of 20 healthy, full term, male infants at a postnatal age of 7 days the NAG:creatinine ratio was significantly higher in the preterm group, the measurements having been taken from single urine spot samples. We suggest that this variable be used in the evaluation of renal tubular integrity during the neonatal period.     

Urinary aquaporin-2 excretion in preterm and full-term neonates

The study was undertaken to define the role of aquaporin-2 (AQP2) in renal concentrating performance by measuring urinary AQP2 excretion and urine osmolality in healthy preterm and full-term neonates during early postnatal life. Random urine samples were obtained from 9 full-term newborn infants (mean birth weight 3,218 g, mean gestational age 39.2 weeks) at postnatal ages of 1, 3 and 5 days. Five premature infants with a mean birth weight of 1,570 g and mean gestational age of 30.6 weeks were studied at the end of the 1st week and then weekly up to the 6th week. Urine osmolality (Knauer osmometer), creatinine (modified Jaffé's method) and AQP2 concentrations (radioimmunoassay) were measured. In full-term neonates, urinary AQP2 excretion showed no consistent changes over the age period studied, while urine osmolality decreased significantly with advancing age. In premature infants, urinary AQP2 excretion remained practically unchanged during the first 4 weeks followed by an abrupt increase thereafter. Urine osmolality did not follow the developmental pattern of AQP2 excretion; its mean values varied only from 78 +/- 39 to 174 +/- 146 mosm/l during the experimental period. It is concluded that during the early postnatal period, urinary AQP2 excretion does not serve as a direct marker of the renal action of AVP and the renal capacity to concentrate urine.     

Zinc status of infants with fetal alcohol syndrome

Plasma and urinary zinc levels were examined in 6 infants with fetal alcohol syndrome to determine whether zinc deficiency, if present in fetal alcohol syndrome patients, is secondary to an increased urinary zinc excretion. Six infants born to nonalcoholic mothers served as controls. There was no significant difference in creatinine clearance, urine flow rate, or plasma albumin concentrations between the two groups. Plasma concentrations of zinc were significantly lower in fetal alcohol syndrome patients (62.5 +/- 2.8 micrograms/dl) in comparison to controls (71 +/- 1.8 microgram/dl), (p = 0.0001). Urinary excretion of zinc in fetal alcohol syndrome patients averaged 646 +/- 125 micrograms/24 h, significantly higher than in control subjects (76.6 +/- 22 micrograms/24 h), (p = 0.0001). Thus (1) lower plasma zinc levels are present in infants with fetal alcohol syndrome and (2) increased urinary zinc excretion appears to be responsible for decreased plasma zinc concentrations.