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Related Experiment Videos

Renal acid excretion in early infancy

F Manz1, H Kalhoff, T Remer

  • 1Research Institute of Child Nutrition, Dortmund, Germany.

Pediatric Nephrology (Berlin, Germany)
|April 1, 1997
PubMed
Summary

Infants are prone to metabolic acidosis due to immature kidney function and formula feeding. Alkali therapy and modified formulas can prevent or treat this condition, which may be an evolutionary adaptation.

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Area of Science:

  • Neonatal physiology
  • Pediatric nephrology
  • Biochemistry

Background:

  • Infants, especially preterm and small-for-gestational-age, exhibit a predisposition to metabolic acidosis.
  • This is linked to immature renal acid excretion capacity and high acid load from standard infant formulas.
  • Persistent maximum renal net acid excretion (NAE) has been observed in some infants, even with normal blood acid-base status.

Purpose of the Study:

  • To investigate the complexities of acid-base metabolism disorders in early infancy.
  • To explore the implications of persistent maximum renal NAE in vulnerable infant populations.
  • To evaluate the efficacy of alkali therapy and formula modification for managing metabolic acidosis.

Main Methods:

  • Analysis of acid-base metabolism in early infancy.
  • Monitoring renal net acid excretion (NAE) in preterm and small-for-gestational-age infants.
  • Assessment of alkali therapy and modified formula interventions.

Main Results:

  • Incipient late metabolic acidosis is identified as a mixed disorder with maximum renal NAE.
  • Alkali therapy proves highly effective, diagnosable via urine pH screening.
  • Modified formulas reducing renal NAE, similar to human milk, offer a preventive strategy.

Conclusions:

  • Infant metabolic acidosis is influenced by renal immaturity and nutrition.
  • Alkali therapy and formula adjustments are effective management strategies.
  • Low renal acid excretion capacity may be an evolutionary adaptation for energy conservation during breastfeeding.

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