Growth patterns of the heart and kidney suggest inter-organ collaboration in facultative fetal growth.

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.