ArticlePediatric nephrology (Berlin, Germany)2009
Urinary vitamin A excretion in very low birth weight infants.
Article in Pediatric nephrology (Berlin, Germany), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Effect of vitamin A supplementation on the urinary retinol excretion in very low birth weight infants.European journal of pediatrics · 2016Article
- Characterization of the vitamin A transport in preterm infants after repeated high-dose vitamin A injections.European journal of clinical nutrition · 2014Article
- Vitamin A deficiency associated with urinary retinol binding protein wasting in Dent's disease.Pediatric nephrology (Berlin, Germany) · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Vitamin A (VA) deficiency in very low birth weight (VLBW) infants is associated with an increased risk for disorders related to kidney and lung maturation and function. VA losses through increased urinary retinol (ROH) excretion might contribute to this deficiency risk. The mechanism accounting for ROH loss in the urine has not yet been clarified. The aim of this study was to assess the excretion of ROH, retinol-binding protein 4 (RBP4) and transthyretin (TTR) in urine from VLBW infants in comparison with that in term infants in relation to kidney function. Urine specimens were collected from 15 VLBW infants (birth weight < 1,500 g) as well as from 20 term infants during the first 2 days after birth. ROH in urine was detectable in 14 of the 15 VLBW infants at a median concentration of 234 nmol/g creatinine. In the group of term infants, 17 of the 20 excreted ROH, but at an approximately five-times lower concentration (P < 0.001). Excretion of RBP4 and TTR was also much higher in VLBW infants (both P< 0.001). The urinary ROH excretion in VLBW infants may be related to the impaired tubular handling of its carrier proteins RBP4 and TTR. Thus, ROH excretion might contribute to an increased risk of VA deficiency, especially in VLBW infants.
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