Deficient fetal growth is also associated with postnatal structural and functional renal changes. In a review by Luyckx and Brenner (2015), birthweight abnormalities were evaluated for linkage with disordered nephrogenesis, renal dysfunction, chronic kidney disease, and hypertension. Both low and high birthweight, as well as maternal obesity and gestational diabetes, afect in-utero development of the kidney and its health into adulthood. However, other variables that include childhood nutrition, acute kidney injury, excessive childhood weight gain, and obesity also worsen long-term renal function.
Particularly in women with diabetes and elevated cord blood levels of IGF-1, fetal overgrowth is associated with greater neonatal fat mass and morphological heart changes. Pedersen (1954) irst proposed that hyperglycemia leads to fetal hyperinsulinemia and fetal overgrowth. This has been extended to organ dysmorphia, for example, increased interventricular septal thickness in neonates of mothers with gestational diabetes (nan, 2011; Garcia-Flores, 2011). he cardiopulmonary vasculature is also adversely afected by diabetes in pregnancy. In 3277 cases of persistent pulmonary hypertension of the newborn (PPHN), maternal obesity, diabetes, and both deficient and excessive fetal growth were independent risk factors (Steurer, 2017). Longterm consequences of fetal overgrowth from obesity and diabetes are discussed in Chapters 48 (p. 941) and 57 (p. 1097).
Numerous reports have described accelerated fetal pulmonary maturation in complicated pregnancies associated with growth restriction (Perelman, 1985). One possible explanation is that the fetus responds to a stressed environment by augmenting adrenal glucocorticoid secretion, which leads to accelerated fetal lung maturation (Laatikainen, 1988). Although this concept pervades modern perinatal thining, evidence to support it is negligible.
To examine this hypothesis, Owen and associates (1990) analyzed perinatal outcomes in 178 women delivered because of hypertension. hey compared these with outcomes in newborns of 159 women delivered because of spontaneous preterm labor or ruptured membranes. They concluded that a "stressed" pregnancy did not confer an appreciable survival advantage. Similar findings were described by Friedman and colleagues (1995) in women with severe preeclampsia. Two studies from Parkland Hospital also substantiate that the preterm infant accrues no apparent advantages from fetal-growth restriction (McIntire, 1999; Tyson, 1995).
Risk factors for impaired fetal growth include potential abnormalities in the mother, fetus, and placenta. hese three "compartments" are depicted in Figure 44-4. Some of these factors are known causes of fetal-growth restriction and may afect more than one compartment. For instance, cytomegalovirus infections can afect the fetus directly. In contrast, bacterial infections such as tuberculosis may have signiicant maternal efects that lead to poor fetal growth. Similarly, malaria, a protozoal infection, is a recognized cause of fetal-growth restriction (Briand, 2016). Importantly, many causes of diminished fetal growth are prospectively considered risk factors, because impaired fetal growth is not consistent in all afected women.