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Updated: Aug 19, 2026

In Utero Intra-cardiac Tomato-lectin Injections on Mouse Embryos to Gauge Renal Blood Flow
Published on: February 4, 2015
Growth patterns of the heart and kidney suggest inter-organ collaboration in facultative fetal growth
Michelle Lampl1, Christopher W Kuzawa, Philippe Jeanty
1Department of Anthropology, Emory University, 1557 Dickey Drive, Atlanta, Georgia 30322, USA. Mlampl@emory.edu
Insights
Maternal smoking during pregnancy alters fetal kidney and heart growth. Smoke-exposed fetuses showed distinct changes in organ size and timing, suggesting adaptive responses to prenatal stress.
Area of Science:
- Obstetrics and Gynecology
- Fetal Development
- Cardiovascular Physiology
Background:
- Maternal smoking during pregnancy is linked to adverse offspring outcomes, including hypertension.
- Previous research primarily used animal models to study smoke exposure effects on organ development.
- Human data on the specific anatomical changes in fetal organs due to maternal smoking are limited.
Purpose of the Study:
- To longitudinally assess fetal kidney and heart growth trajectories and morphology in relation to maternal smoking.
- To identify specific anatomical alterations in fetal organs resulting from in utero smoke exposure.
- To explore potential mechanisms linking prenatal smoke exposure to postnatal sequelae.
Main Methods:
- Longitudinal growth study involving 34 healthy maternal/fetal pairs (24 non-smokers, 10 smokers) from 13 weeks of gestation.
- Utilized curve fitting and mixed-effects models for repeated measures to analyze organ growth patterns.
- Documented fetal kidney and heart growth parameters including width, thickness, length, and volume.
Main Results:
- Maternal smoking was associated with significantly different fetal kidney growth patterns, initially wider and thicker, then proportionately thinner.
- Fetal cardiac growth showed a reverse pattern, with accelerated volume and width after 30 weeks gestation.
- Observed changes in organ morphology suggest compensatory growth in response to smoke exposure during mid-gestation.
Conclusions:
- In utero smoke exposure alters the size and timing of fetal heart and kidney development.
- These anatomical changes provide a potential mechanism for previously reported negative outcomes associated with maternal smoking.
- Longitudinal ultrasound assessment is crucial for understanding fetal organ-level responses to prenatal stressors.
Abstract:
Maternal smoking during pregnancy has been associated with a number of negative sequelae among offspring, including elevated postnatal blood pressure. While animal studies have described organ level alterations with smoke exposure, human data have been more limited. Thirty-four healthy maternal/fetal pairs (24 nonsmokers, 10 smokers) participated in a longitudinal growth study from the thirteenth week of pregnancy to document fetal kidney and heart growth trajectories and morphology. Curve fitting followed by a mixed model for repeated measures identified significantly different growth patterns in kidney width, thickness, length, and volume growth with exposure: the smoke-exposed fetal kidney was wide and thick compared to the unexposed kidney during the second and early third trimester, declining to proportionately thin kidneys for length and width subsequently. Cardiac growth in width and volume followed a reverse pattern: a surge in cardiac volume occurred after 30 weeks with acceleration in cardiac width, resulting in a heart that was wide for length and for fetal weight. Smoke exposure altered fetal growth in size and timing of the heart and kidneys during midgestation, with changes in organ morphology suggesting compensatory growth. These are the first data providing anatomical evidence of altered renal/cardiac volume relationships that may provide a mechanism to previously reported sequelae of in utero smoke exposure. They suggest that cell-level adaptive responses to hypoxia and/or chemical insults are operative and illustrate the importance of longitudinal ultrasound to directly assess the organ-level growth response of the human fetus to a prenatal stress, in lieu of relying on birth outcome measures.
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