Maternal diabetes during pregnancy, including pre-gestational and gestational diabetes mellitus (DM), can significantly affect fetal development, particularly in the kidneys. This study aimed to investigate the effects of maternal diabetes on fetal kidney size, parenchymal thickness, and renal artery hemodynamics using ultrasonography. A total of 128 pregnant women were enrolled and classified into pre-gestational DM (n = 28), gestational DM (n = 36), and control (n = 64) groups. Fetal kidney measurements, including anteroposterior, mediolateral, and longitudinal diameters as well as renal parenchymal thickness (RPT) and renal artery pulsatility index (PI), were assessed between 28 and 38 weeks of gestation. Fetal kidney volumes and their ratios to estimated fetal weight (EFW) and abdominal circumference (AC) were significantly lower in both the pre-gestational and gestational DM groups than in the controls (p < 0.05). However, no significant differences were observed in the RPT/AC ratios or renal artery PI among the groups. Furthermore, no significant correlations were found between maternal hemoglobin A1c (HbA1c) levels and fetal kidney or blood flow parameters. These findings suggest that maternal diabetes alters fetal kidney growth patterns relative to the overall fetal size, potentially reflecting developmental programming that may affect nephron endowment and long-term renal health. The lack of significant differences in RPT/AC ratios and renal artery PI may be attributed to effective diabetes management or limitations in detecting subtle changes using the current ultrasound methodologies. Further longitudinal studies with larger cohorts and postnatal follow-up are warranted to clarify long-term renal outcomes and explore the precise mechanisms underlying these developmental changes.

Maternal insufficiency during fetal development can have long-lasting effects on the offspring, most notably on nephron endowment. In polycystic kidney disease (PKD), variability in severity of disease is observed and maternal environment may be a modifying factor. In this study, we first established that in a rodent model of PKD, the Lewis polycystic kidney (LPK) rat’s nephron numbers are 25% lower compared with wildtype animals. We then investigated the effects of prenatal and postnatal maternal environment on phenotype and nephron number. LPK pups born from and raised by homozygous LPK dams (control) were compared with LPK pups cross-fostered onto heterozygous LPK dams to improve postnatal environment; with LPK pups born from and raised by heterozygous LPK dams to improve both prenatal and postnatal environment and with LPK pups born from and raised by Wistar Kyoto-LPK heterozygous dams to improve both prenatal and postnatal environment on a different genetic background. Improvement in both prenatal and postnatal environment improved postnatal growth, renal function and reduced blood pressure, most notably in animals with different genetic background. Animals with improved postnatal environment only showed improved growth and blood pressure, but to a lesser extent. All intervention groups showed increased nephron number compared with control LPK. In summary, prenatal and postnatal environment had significant effect in delaying progression and reducing severity of PKD, including nephron endowment.