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Urinary vitamin A excretion in very low birth weight infants

Britta Nagl1, Andrea Loui, Jens Raila

  • 1Department of Physiology and Pathophysiology, Institute of Nutritional Science, University of Potsdam, Potsdam, Germany. britta.nagl@uni-potsdam.de

Insights

Very low birth weight infants show higher urinary retinol losses, potentially increasing their risk for Vitamin A deficiency. This is linked to impaired kidney handling of carrier proteins like RBP4 and TTR.

Area of Science:

  • Neonatal Medicine
  • Nutritional Science
  • Pediatric Nephrology

Background:

  • Vitamin A (VA) deficiency poses risks to kidney and lung development in very low birth weight (VLBW) infants.
  • Increased urinary retinol (ROH) excretion is a suspected contributor to VA deficiency in VLBW infants.
  • The precise mechanism of urinary ROH loss remains unclear.

Purpose of the Study:

  • To investigate urinary excretion of retinol (ROH), retinol-binding protein 4 (RBP4), and transthyretin (TTR) in VLBW infants.
  • To compare ROH, RBP4, and TTR excretion in VLBW infants versus term infants.
  • To explore the relationship between urinary ROH excretion and kidney function in these infant groups.

Main Methods:

  • Urine samples collected from 15 VLBW infants (<1,500 g) and 20 term infants within 48 hours of birth.
  • Quantification of urinary ROH, RBP4, and TTR levels.
  • Analysis of urinary concentrations relative to creatinine and comparison between VLBW and term infant groups.

Main Results:

  • Retinol (ROH) was detected in 93% of VLBW infants at a median concentration of 234 nmol/g creatinine.
  • Term infants also excreted ROH (85%), but at a significantly lower concentration (approximately five times less than VLBW infants).
  • Urinary RBP4 and TTR levels were significantly higher in VLBW infants compared to term infants.

Conclusions:

  • Elevated urinary ROH excretion in VLBW infants may stem from impaired tubular reabsorption of carrier proteins RBP4 and TTR.
  • Increased urinary ROH loss could be a contributing factor to Vitamin A deficiency in VLBW infants.
  • Further research is needed to elucidate the mechanisms and clinical implications of these findings.

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