Acid Excretion In Infants Research Articles

Melamine Toxicity

Melamine contamination of infant formula in China and its health effects highlight the safety of the global food supply especially as it relates to formula-fed infants. Melamine is a widely used industrial chemical not considered acutely toxic with a high LD(50) in animals. The data available on acute and chronic human exposure to melamine have been limited and extrapolated from animal data. Pet food contamination in 2004 and 2007 showed stone formation and illness in animals when melamine was co-ingested with cyanuric acid. The recent outbreak in infants showed that melamine ingested in large doses may cause stones and illness without significant ingestion of cyanuric acid or other melamine-related chemicals. This may be due to increased uric acid excretion in infants and formation of melamine-uric acid stones. Diagnosis and treatment of infants exposed to melamine requires further study. Clinical signs and symptoms in infants are nonspecific. The stones may be radiolucent and are not consistently seen on ultrasound. The use of alkalinization of the urine for treatment has been proposed, but is of unproven benefit. The FDA and other regulatory agencies have recommended acceptable levels of melamine in foods for consumption. Melamine ingestion has been implicated in stone formation when co-ingested with cyanuric acid, but will cause urinary stones in infants when large amounts of melamine alone are ingested.

Amino acid excretion in infants and children.

Amino acid excretion in infants and children.

Influence of Purine Intake on Uric Acid Excretion in Infants Fed Soy Infant Formulas

Objective: These studies tested the hypothesis that increasing intake of purines, delivered as RNA from soy protein-based infant formula, would increase urinary uric acid excretion in infants.Methods: Study One examined the influence of feeding on serum uric acid in a total of 178 infants from four separate trials with infants fed commercial and experimental soy-based and milk-based infant formulas or human milk. Studies Two and Three compared the effect of a standard purine soy formula (STD Purine; 180 mg purines/L from RNA) and a reduced purine soy formula (Reduced Purine; 65 mg purines/L; 26 mg/L from RNA and 39 mg/L from ribonucleotides) on urinary uric acid excretion in infants. In Study Two, 11 infants ranging in age from 16 to 128 days of age were fed both formulas in a random crossover design. Complete 72-hour urine collections were done at the end of each 11-day feeding period. Urinary uric acid excretion was expressed as mmol/day. In Study Three, 33 infants were enrolled before eight days of age and randomized to one of the formulas one week later. Spot urine samples were collected at 28 and/or 56 days of age and urinary uric acid concentration was expressed as mmol/mmol creatinine.Results: In Study One, each of the feedings resulted in mean serum uric acid levels within normal reference ranges. Soy formula led to higher serum uric acid levels than human milk, and human milk to levels indistinguishable from cow milk-based formulas. In Study Two, infants excreted significantly more uric acid in the urine when fed the STD Purine formula compared to the Reduced Purine formula (0.86±.04 vs. 0.57±.04 mmol/d) (p=0.006). In Study Three, infants fed the STD Purine formula had a significantly higher concentration of uric acid in their urine compared to those fed the Reduced Purine formula (2.1±0.2 vs. 1.4±0.1 mmol uric acid/mmol creatinine) (p=0.0001).Conclusion: These data indicate that healthy infants can digest RNA and subsequently absorb the liberated purine ribonucleotides as determined by urinary uric acid concentration.

Increased urine methylmalonic acid excretion in infants with apnoeas.

Journal of Inherited Metabolic DiseaseVolume 21, Issue 1 p. 86-87 Article Increased urine methylmalonic acid excretion in infants with apnoeas R. Artuch, R. ArtuchSearch for more papers by this authorM. Calvo, M. CalvoSearch for more papers by this authorA. Ribes, A. RibesSearch for more papers by this authorF. Camarasa, F. CamarasaSearch for more papers by this authorM. A. Vilaseca, M. A. VilasecaSearch for more papers by this author R. Artuch, R. ArtuchSearch for more papers by this authorM. Calvo, M. CalvoSearch for more papers by this authorA. Ribes, A. RibesSearch for more papers by this authorF. Camarasa, F. CamarasaSearch for more papers by this authorM. A. Vilaseca, M. A. VilasecaSearch for more papers by this author First published: 01 February 1998 https://doi.org/10.1023/A:1005383919335Citations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume21, Issue1February 1998Pages 86-87 RelatedInformation

Effects of Different Formula Feeds on the Developmental Pattern of Urinary Bile Acid Excretion in Infants

Summary:The excretion of bile acids in urine was followed prospectively during the first year of life in 17 infants fed different diets from the age of 3 to 10 days. Eight infants were breast‐fed, four were fed formulas that were based on adapted cow's milk, and five were fed a formula that was based on soy protein isolate. The formulas had higher protein concentrations than human milk; had different types of proteins, and had not been supplemented with taurine. Urinary bile acids were determined by gas‐liquid chromatographic/mass spectrometric analyses of 24‐h urinary samples collected at 1–12 days (only formula‐fed infants) and at 1, 3, 6, 9, and 12 months of age. The results showed a higher urinary bile acid excretion at 3 months of age in both formula groups than in the breastfed infants. A deficiency of dietary taurine during formula‐feeding did not seem to limit the formation of taurine conjugates during the first month of life. The developmental pattern of urinary bile acid excretion during the first year differed according to the type of feeding. Isomers of cholic and chenodeoxycholic acid appeared in the urine of all breast‐fed infants at 6 to 12 months of age. These metabolites, assumed to be the first metabolites derived from the developing gut flora of the infants, appeared at an earlier age and in higher amounts in both formula groups compared to breast‐fed infants. Bile acids lacking a 7‐hydroxy group, known to be formed by the intestinal flora, appeared in infants in all feeding groups later than the isomers. The results of the study imply that the early introduction of formula may modify bile acid metabolism in infants.

Urinary methylmalonic acid excretion in infants fed formula or human milk

Serum vitamin B-12 and urinary methylmalonic acid (MMA) concentrations were determined in 62 healthy infants aged 1-6 mo. Urinary MMA was inversely correlated with serum vitamin B-12 concentrations (r = -0.550, p less than 0.001); serum vitamin B-12 was higher (p less than 0.001) and urinary MMA concentrations were lower (p less than 0.001) in formula-fed infants than in infants fed human milk (from the breast). Human-milk-fed infants who had received supplemental formula had higher serum vitamin B-12 concentrations than did infants exclusively fed human milk. It is not clear whether the serum vitamin B-12 and urinary MMA concentrations in infants fed human milk reflect biochemical deficiency of vitamin B-12, and the clinical significance of these findings needs to be investigated.

Renal acid excretion in infants with the respiratory distress syndrome.

Extract: Acid-base balance in blood and hydrogen ion, phosphorus concentrations, and acid-base excretion in urine were measured in 10 infants with respiratory distress syndrome (RDS), in 8 control full term infants, and in 7 control premature infants on days 1, 2, and 3 of life. Infants with RDS were acidemic in comparison with full term and premature control infants. Hydrogen ion concentrations in urine were similar for premature control subjects and acidemic infants with RDS but lower in comparison with those of full term control infants. The inability of infants with RDS, in the face of acidemia, to create an appreciable urine to plasma hydrogen ion concentration gradient provided evidence for a renal tubular deficiency in hydrogen ion secretion. Phosphate levels in urine and, as a result, titratable acid were usually low in the three groups of infants. Relative phosphaturia did occur in some infants with RDS, but, because of the deficiency in hydrogen ion secretion, urinary phosphate was often not utilized as titratable acid. At high urinary concentrations of hydrogen ion (above 400 μmEq/liter), control premature infants and acidemic infants with RDS excreted urine having lower ammonium concentration than that found in control full term infants. The inability of infants with RDS with acidemia to excrete ammonium when hydrogen ion concentrations in urine were high was evidence of a renal tubular deficiency in ammonia production. Infants with RDS differed from control premature infants by having high hydrogen ion and bicarbonate concentrations in blood in relation to higher blood PCO2 values. In addition, at low hydrogen ion concentrations in urine, infants with RDS excreted urine that contained higher concentrations of bicarbonate than that found in control premature infants. Because infants with RDS did not excrete ammonium, they could not compensate for the increased acid load and bicarbonate excretion associated with respiratory acidemia. In addition, they could not compensate for the low titratable acid, which resulted from decreased excretion of phosphate, characteristic of the newborn period. Infants with RDS did not respond to acidemia by increasing net acid excretion in urine beyond that excreted by control infants. Indeed, some infants with RDS inappropriately excreted base, thereby aggravating their already existing acidemia. Speculation: Low gestational and postnatal age is the likely etiologic factor responsible for the decreased capacity for urinary acid excretion seen in infants with RDS. The apparent improvement in renal tubula hydrogen ion secretion with increasing gestational age may be associated with maturation of an enzyme system such as carbonic anhydrase. Likewise, the apparent improvement in renal tubular ammonia production with increasing gestational age may occur in relation to maturation of an enzyme system such as glutaminase.

Uric acid excretion in infants and children

A new paper-chromatographic test for urinary uric acid is described based on the reaction of dichloroquinonechlorimide with uric acid. Mean excretion of uric acid by 2506 infants and children was 0.51 ± 0.37 mg/ml. Differences between boys and girls were not significant. Uric acid excretion increased during the age period from 3 months to 1–2 years and remained fairly constant up to 12–16 years. Uric acid determinations using the standard uricase method showed a high correlation with values obtained by paper chromatography.

Observations on Urocanic Acid and Formiminoglutamic Acid Excretion in Infants with Protein Malnutrition

Compared to healthy infants, over 80 per cent of infants with protein malnutrition excreted excessive quantities of urocanic acid and formiminoglutamic acid (FIGLU) after administration of a relatively large loading dose of histidine. Excessive urinary urocanic acid excretion decreased on refeeding, irrespective of folic acid or vitamin B12supplementation. High urinary urocanic excretion correlated with elevated serum vitamin B12, levels, suggesting that both were associated with hepatocellular damage. All infants with clinical folate deficiency excreted excessive quantities of formiminoglutamic acid after histidine loading, but this excessive excretion could be eliminated by folic acid therapy in only one third of the infants. Many infants with excessive urinary FIGLU had normal serum Lactobacillus casei folate levels and normoblastic bone marrows. Excessive urinary excretion of histidine derivatives by infants with protein malnutrition apparently is dependent on the interaction of a number of factors including folate deficiency, utilization of histidine for protein synthesis and the integrity of the various hepatic enzymes controlling the histidine-glutamic acid pathway.