Phosphorus Intake in Preterm Babies and Variation of Tubular Reabsorption for Phosphate per Liter Glomerular Filtrate

Langhendries, J. P.; François, Ayme; Chedid, Fares; Battisti, Oreste; Bertrand, J. M.; Senterre, J

doi:10.1159/000243820

Cited by 11 publications

(6 citation statements)

References 11 publications

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“…Several studies reported on Tp/GFR in more mature infants. In infants at 30-35 weeks GA, a median Tp/GFR value of 2.06 mmol/l was reported [7]. All of the values reported correspond well to the values we found in the group of 26-31 weeks GA. Several mechanisms could be responsible for the low Tp/GFR values in the infants 23-25 weeks GA. First, the extremely premature kidney could reabsorb phosphate poorly, even in the absence of kidney damage or phosphaturic medication.…”

Section: Discussionsupporting

confidence: 88%

Renal phosphate handling of premature infants of 23?25 weeks gestational age

Hellstern

Pöschl

Linderkamp

2003

Pediatric Nephrology

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Premature infants with low serum phosphate concentrations (<2 mmol/l) are at risk for osteopenia. Therefore, serum phosphate levels in premature infants should be kept above 2 mmol/l. Premature infants of 26-31 weeks gestational age (GA) have renal phosphate threshold concentrations (Tp/GFR) in the range of normal serum phosphate values (2 mmol/l). Therefore, these infants show significant urinary phosphate excretion only when serum phosphate levels are normal, and urinary phosphate excretion can be used to monitor phosphate supplementation. However, few data are available on extremely premature infants of 23-25 weeks GA. The objective of this study was to compare Tp/GFR levels in infants of 23-25 weeks GA to those in infants of 26-31 weeks GA. We retrospectively evaluated case notes of 12 infants of 23-25 weeks GA and compared them to 19 infants of 26-31 weeks GA. Tp/GFR was calculated from simultaneous measurements of urinary phosphate, urinary creatinine, serum phosphate, and serum creatinine. Tp/GFR values 3-5 weeks postnatally were lower in infants of 23-25 weeks GA (1.06+/-0.36 mmol/l, p<0.001) than in infants of 26-31 weeks GA (1.76+/-0.26 mmol/l). Near term (35-37 weeks postmenstrual age), there was no significant difference between Tp/GFR values in infants of 23-25 weeks GA (1.83+/-0.32 mmol/l) and in infants of 26-31 weeks GA (2.05+/-0.22 mmol/l). We conclude that at 3-5 weeks postnatally, infants of 23-25 weeks GA are at risk for low Tp/GFR values, leading to urinary phosphate excretion even in the presence of low serum phosphate levels. In these infants, serum phosphate levels should be monitored, and phosphate supplementation should be adjusted to keep serum phosphate levels above 2 mmol/l.

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Section: Discussionsupporting

confidence: 88%

Renal phosphate handling of premature infants of 23?25 weeks gestational age

Hellstern

Pöschl

Linderkamp

2003

Pediatric Nephrology

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“…These mechanisms could still be immature and contribute to higher Ox/Cr ratios in preterm infants. The higher Ca excretion in preterm infants could be secondary to lower urinary phosphate reabsorption leading to phosphate depletion despite higher dietary phosphate [3,8,10].…”

Section: Discussionmentioning

confidence: 99%

Influence of nutrition on urinary oxalate and calcium in preterm and term infants

et al. 1997

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Few data for normal urinary oxalate (Ox) and calcium (Ca) excretion related both to gestational age and nutritional factors have been reported in preterm or term infants. We therefore determined the molar Ox and Ca to creatinine (Cr) ratios in spot urines from 64 preterm and 37 term infants aged 1-60 days, either fed formula or human milk (HM). Only vitamin D was supplemented; renal or metabolic diseases were excluded. Urinary Ox/Cr ratio was higher in preterm than in term infants, both when formula fed (1st month 253 vs. 180 mmol/mol and 2nd month 306 vs. 212 mmol/mol; P<0.05) or HM fed (206 vs. 169 mmol/ mol and 283* vs. 232 mmol/mol; *P<0.05). Ox/Cr was also higher in formula- than HM-fed preterm infants. The ratio increased during the first 2 months of life irrespective of nutrition. Urinary Ca/Cr ratio was comparable in all groups during the 1st month of life, except for a lower (P < 0.05) value in term infants fed HM (0.10 mol/mol). It increased in all groups during the 2nd month of life, being highest in HM-fed preterm infants (1.86 mol/mol). In conclusion, urinary Ox and Ca excretion is influenced by both gestational age and nutrient intake in preterm and term infants.

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“…Considering that calcium soft tissue retention is negligible, renal calcium load is highly dependent on the bone calcium deposition associated with phosphorus in the form of hydroxyapatite (Ca 10 (PO 4 ) 6 (OH) 2 ) containing a molar Ca:P ratio of 1.67 (2.15 wt/wt). Thus, the main determinant of calcium urinary loss in preterm and term neonates is a relative phosphorus depletion [21,22]. This has been illustrated in balance studies performed in growing preterm infants fed human milk.…”

Section: Hypercalciuria In Preterm Infants Fed Human Milkmentioning

confidence: 98%

Nutrition and kidney in preterm infant

Curtis

Rigo²

2012

The Journal of Maternal-Fetal & Neonatal Medicine

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In pre- and post-natal period nutrition can influence the function of many organs, including the kidneys. Intrauterine growth restriction and low weight at birth are associated with reduced nephron number, a risk factor for later cardiovascular and renal diseases. The development of such adult diseases may be favored, in animals, by additional risk factors, including postnatal overnutrition and/or rapid postnatal growth. In preterm infants, during the first weeks of life, high values of serum urea are presents due to immaturity of the renal function. Thus the urea cannot be used in the first weeks of life as a parameter to evaluate the adequacy of protein intake. In comparison with older infants, healthy preterm infants, fed on human milk and adapted formulas, show a lower renal solute load because the higher growth rate associated with a raised nitrogen and mineral retention rate. Preterm infants are vulnerable to disturbances of acid-base metabolism, with a predisposition to metabolic acidosis due to a transient age-related low renal capacity for net acid excretion.

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Phosphorus Intake in Preterm Babies and Variation of Tubular Reabsorption for Phosphate per Liter Glomerular Filtrate

Cited by 11 publications

References 11 publications

Renal phosphate handling of premature infants of 23?25 weeks gestational age

Renal phosphate handling of premature infants of 23?25 weeks gestational age

Influence of nutrition on urinary oxalate and calcium in preterm and term infants

Nutrition and kidney in preterm infant

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