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Published on: June 29, 2013
Perinatal lipocalin-2 profile at the extremes of fetal growth
Aimilia Eirini Papathanasiou1, Ariadne Malamitsi-Puchner1, Stavroula Gavrili2
1Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Insights
Lipocalin-2 (LCN-2) levels in cord blood are higher than in maternal serum and may indicate fetal origin and a role in intrauterine growth. Elevated cord blood LCN-2 in growth-restricted neonates suggests potential kidney issues.
Area of Science:
- Neonatal research
- Endocrinology
- Perinatal medicine
Background:
- Lipocalin-2 (LCN-2) is an osteoblast-secreted hormone involved in immunity, inflammation, and metabolic homeostasis.
- LCN-2 is a biomarker for acute kidney injury in neonates.
- Fetal growth impacts LCN-2 concentrations in maternal serum, cord serum, and breast milk.
Purpose of the Study:
- Investigate the impact of fetal growth on LCN-2 concentrations.
- Analyze associations between LCN-2 and perinatal parameters.
Main Methods:
- Measured LCN-2 concentrations using ELISA in 80 mothers and their neonates (AGA, LGA, IUGR).
- Classified neonates by customized weight centiles.
- Correlated LCN-2 levels with birth weight, centile, gender, maternal age, and delivery mode.
Main Results:
- Maternal serum LCN-2 was higher in AGA infant deliveries.
- Cord serum LCN-2 exceeded maternal levels and was elevated in IUGR vs. LGA neonates.
- Breast milk LCN-2 was low and consistent across groups.
- Negative correlation between cord LCN-2 and customized centiles (r: -0.304, p = .007).
Conclusions:
- Higher cord LCN-2 suggests fetal origin and a role in intrauterine growth.
- Elevated cord LCN-2 in IUGR may indicate reduced nephron endowment or kidney damage.
- Low LCN-2 in breast milk suggests maternal circulation to milk is not affected by intrauterine growth pathology.
Background:
Lipocalin-2 (LCN-2) has been identified as an osteoblast-secreted hormone regulating immunity, inflammation and metabolic homeostasis and has emerged as a diagnostic and prognostic biomarker for acute kidney injury in neonates. We investigated the impact of fetal growth on antepartum maternal serum, cord serum and breast milk LCN-2 concentrations and the associations of the latter with perinatal parameters.
Methods:
Maternal serum, cord serum and breast milk LCN-2 concentrations were measured by ELISA in samples from 80 mothers who delivered 40 appropriate (AGA), 20 large for gestational age (LGA) and 20 intrauterine growth restricted (IUGR) neonates, classified by customized weight centiles. LCN-2 concentrations were associated with birth weight, customized centile, gender, maternal age and delivery mode.
Results:
Antepartum maternal serum LCN-2 concentrations were significantly higher in women delivering AGA infants compared to the other two groups. Cord blood LCN-2 concentrations were significantly higher compared to maternal ones; furthermore, they were significantly elevated in the IUGR group compared to the LGA one (p = .019). Lowest concentrations were detected in breast milk, which did not differ between the three growth groups. A negative correlation was documented between cord blood LCN-2 concentrations and customized centiles (r: -0.304, p = .007).
Conclusions:
The higher cord serum LCN-2 concentrations, compared to maternal ones, may point to its fetal origin and potential role in intrauterine growth. The negative correlation of cord LCN-2 concentrations with customized centiles, possibly implies reduced nephron endowment/subclinical kidney damage in IUGR neonates. The extremely low LCN-2 breast milk concentrations could imply that the secretion of LCN-2 from maternal circulation to breast milk is not influenced by factors leading to intrauterine growth pathology.
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