Yun Ji Jung

Objectives: Prenatal diagnosis of horseshoe kidney (HSK), a common congenital renal fusion anomaly of the upper urinary tract, remains challenging. Most cases are identified only after birth; however, the clinical significance of prenatal detection and its impact on postnatal outcomes remains unknown. Methods: We investigated infants with postnatally confirmed HSK born at a tertiary referral center between January 2009 and August 2025. Prenatal ultrasonographic findings and postnatal outcomes were reviewed. Patients were classified into three groups according to prenatal detection status: missed HSK (group 1), prenatally detected renal abnormalities without recognition of HSK (group 2), and prenatally identified HSK (group 3). Perinatal outcomes, postnatal urological complications, renal function, and associated anomalies were compared. Results: Overall, 29 infants were included in this study. Perinatal outcomes, including gestational age at delivery, birth weight, preterm birth, Apgar scores, need for ventilatory support, and neonatal sex, did not differ significantly among the groups. Hydronephrosis and renal scarring were more frequently observed in group 2 than in the other groups. Other urological outcomes, renal function parameters, and mortality rates were comparable between the groups. Conclusions: This adds to the limited longitudinal evidence linking the prenatal to postnatal period and evaluating the full spectrum of prenatal detection in HSK, as well as its association with postnatal outcomes. Postnatal outcomes are closely associated with the presence of renal abnormalities. Therefore, prenatal imaging is more appropriate for identifying associated renal abnormalities than for establishing a definitive diagnosis of HSK.

Background: Placenta accreta spectrum (PAS), an abnormal placental invasion into the myometrium or beyond the uterine serosa, is associated with adverse pregnancy outcomes. Placenta previa is the most significant individual risk factor for PAS, and Ultrasonography (US) and Magnetic resonance imaging (MRI) are widely used to detecting PAS. However, limited data exist on the effectiveness of US and MRI in predicting maternal and neonatal morbidity. This study evaluated the utility of these imaging modalities, not only in detecting PAS but also in predicting adverse perinatal outcomes. Methods: This retrospective cohort study included 150 pregnant women with placenta previa who underwent US and MRI at a tertiary hospital between December 2019 and December 2023. PAS was diagnosed clinically or histopathologically after delivery. The predictive performance of US, MRI, and their combination was assessed using McNemar’s test, receiver operating characteristic analysis, and trend analysis. Results: Forty-one patients were diagnosed with PAS. The PAS group had significantly higher rates of prior caesarean section, maternal hemorrhagic outcomes, and neonatal complications than the non-PAS group. PAS-suspected on US group also showed increased estimated blood loss (EBL) and number of transfusion units administered, as well as a higher incidence of transfusion requirement, use of intrauterine balloon tamponade, hysterectomy, preterm birth before 37 weeks of gestation, neonatal ventilatory support and 1-minutes Apgar scores (AS) <7 compared to those with PAS-unsuspected on US group. PAS-suspected on MRI group had a significantly increased number of transfusion units administered and higher rates of hysterectomy, maternal ICU admission, preterm birth and neonatal complications. US plus MRI yielded progressively higher detection rates, outperforming either modality alone. A linear trend was observed in the increase of adverse perinatal outcomes when PAS was suspected on both US and MRI. Conclusions: US and MRI showed complementary strengths. US, but not MRI, is informative for predicting higher EBL, transfusion requirement, and use of intrauterine balloon tamponade, whereas MRI, but not US, predicts maternal ICU admission, preterm birth before 34 weeks of gestation, NICU admission, and 5-minute AS <7. Combining both imaging modalities yields better performance than either modality alone in detecting PAS and predicting adverse perinatal outcomes.

Background: Endocrine-disrupting chemicals (EDCs) are environmental pollutants that may impair maternal and fetal health by disrupting hormonal systems, including the thyroid. Both iodine deficiency and excess are associated with thyroid dysfunction and adverse obstetrical outcomes. However, the combined impacts of EDCs and iodine exposure on maternal-fetal thyroid homeostasis remain undetermined. We established the Investigating Birth and Thyroid Outcomes of Maternal-Fetal Environmental Exposures (IBM-E) cohort to prospectively assess the effects of maternal exposures to dietary iodine and EDCs on thyroid function, pregnancy complications, and offspring growth and development.Methods: In this prospective observational study, we aim to enroll 556 pregnant women between 2024 and 2027 at a tertiary hospital in Korea. Maternal blood and urine samples will be collected at six time points, spanning from early pregnancy through 15 months postpartum, with infant samples collected at three time points. EDCs will be quantified using ultra-high performance liquid chromatography-tandem mass spectrometry. Thyroid function and urinary iodine concentration will be measured in both mothers and infants.Results: As of the current interim analyses of 193 mothers and 229 neonates, 15.0% of mothers had thyroid dysfunction and 11.4% developed preeclampsia. Preterm birth occurred in 23.8% of cases, and 16.6% of neonates were small for gestational age.Conclusion: The IBM-E cohort is designed to enable the longitudinal assessment of gestational environmental exposures and their potential impacts on maternal and fetal thyroid function, as well as pregnancy and neonatal outcomes. The findings of this study may inform preventive strategies and guide policy development in perinatal environmental health.

Background/Objectives: Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary renal disorder; it is typically diagnosed in adulthood, but occasionally presents antenatally as very-early onset ADPKD. Despite advances in prenatal ultrasonography, knowledge regarding the postnatal course of fetal ADPKD remains limited, restricting reliable prognostic assessment and prenatal counselling. This study aimed to evaluate the prenatal sonographic features of fetal ADPKD and their correlation with postnatal outcomes. Materials and Methods: We retrospectively reviewed 20 cases of prenatally suspected ADPKD diagnosed at a single tertiary referral center between 2006 and 2024. Prenatal ultrasonographic findings including renal size, cortical echogenicity, corticomedullary differentiation (CMD), and cortical cysts were analyzed and correlated with postnatal clinical and genetic outcomes. Postnatal follow-up data, including renal function and progression to chronic kidney disease (CKD), were collected with a median follow-up of 93.6 months. Results: The most consistent prenatal ultrasonographic findings were increased cortical echogenicity (85%), increased CMD (75%), and renal enlargement (35%), with cortical cysts detected in 45% of cases. Amniotic fluid volume was preserved in most cases (80%). Postnatally, most infants maintained normal or near-normal renal function, although two progressed to CKD. Both CKD cases demonstrated absent CMD on prenatal imaging. Sonographic features resembling autosomal recessive polycystic kidney disease (ARPKD) were associated with adverse outcomes. Although CMD severity showed no correlation with short-term neonatal outcomes, loss of CMD may still serve as a potential early indicator of long-term renal dysfunction. Conclusions: Fetal ADPKD was associated with heterogeneous postnatal outcomes. Loss of CMD and ARPKD-like sonographic appearances may be associated with adverse prognosis, whereas most infants maintained preserved renal function. Early recognition of ADPKD is crucial for accurate counselling, appropriate perinatal management, and long-term surveillance.

During pregnancy, exposure to fine particulate matter (PM_2.5), particularly diesel exhaust particles (DEPs), elevates the risk of placental dysfunction-related pregnancy complications; however, the underlying cellular mechanisms have yet to be fully elucidated. The objective of this study was to assess the effects of PM_2.5 exposure on trophoblast functions and their interaction with endometrial stromal cells. We utilized a three-dimensional (3D) model in which human first-trimester trophoblasts (Sw71) formed blastocyst-like spheroids and were cultured with human endometrial stromal cells (HESCs). Trophoblast proliferation, migration, invasion, and 3D network formation following DEP exposure (0.5–20 μg/mL) were assessed using methyl thiazolyl diphenyl-tetrazolium bromide (MTT), wound healing, migration, and invasion assays. The expression levels of genes related to the epithelial-mesenchymal transition (EMT) were quantified by real-time reverse-transcription quantitative polymerase chain reaction (RT-qPCR). DEP exposure significantly inhibited trophoblast proliferation, migration, and invasion. DEP treatment dysregulated the EMT program by significantly decreasing the expression of key mesenchymal markers (SNAI1, SNAI2, SOX2, and KLF4) while upregulating epithelial markers. These changes may be related to inhibited trophoblast migration toward HESC monolayers and 3D invasive network formation. DEP directly impairs critical trophoblast functions that are essential for successful pregnancy. Disruption of the EMT program represents a molecular mechanism by which traffic-related air pollution contributes to placental dysfunction and pregnancy complications, highlighting the significant reproductive risks posed by ambient air pollution.

Background/Objective: Accurately identifying women at high risk for preterm birth among those with threatened preterm labor (PTL) is crucial for effective interventions or tocolytic management to reduce preterm birth and its complications. This study aimed to determine the predictive value of cervical elastography for preterm delivery before 37 weeks of gestation in patients with threatened PTL and a cervical length greater than 15 mm. Methods: This prospective cohort study included pregnant women presenting with threatened PTL at between 24 and 34 weeks gestation. All participants underwent cervical elastography at diagnosis. We compared cervical elastography parameters between women who delivered spontaneously preterm (<37 weeks) and those who delivered at full term and assessed the ability of these parameters to predict spontaneous preterm delivery. Results: Among the 107 enrolled individuals with threatened PTL and a cervical length of ≥15 mm, 55 (42%) experienced preterm birth (<37 weeks). Internal os stiffness (IOS), internal-to-external os stiffness ratio (IOS/EOS ratio), and elasticity contrast index (ECI) were significantly associated with a risk of preterm birth compared to full-term birth. The IOS/EOS ratio was associated with 10-fold higher odds of preterm birth at <37 weeks (95% confidence interval [CI], 1.82–59.98), and ECI was associated with 1.5-fold higher odds (95% CI, 1.01–2.37). The IOS/EOS ratio demonstrated good predictive value (area under the curve (AUC) = 0.678) and the combination of CL ≤ 25 mm and the IOS/EOS ratio had good diagnostic performance for predicting preterm birth (AUC = 0.708). Conclusions: Cervical elastography using the E-Cervix™ system appears to improve the ability to predict preterm birth in pregnant women with threatened PTL and a cervical length greater than 15 mm.

Background/Objectives: Diagnosing interstitial pregnancy (IP) using ultrasonography can be challenging, as it is often mistaken for eccentrically located intrauterine pregnancy (IUP). In this retrospective cohort study, we aimed to develop a predictive scoring model using multiple clinical factors to enhance the diagnosis of IP and facilitate timely interventions in suspected cases. Methods: We enrolled 63 pregnant women with a diagnosis of suspected IP who visited a single tertiary center between January 2006 and December 2023. Data on the clinical risk factors, symptoms, laboratory test results, and ultrasound findings were analyzed. A statistical predictive score was developed using logistic regression analysis with feature selection based on the least absolute shrinkage and selection operator to optimize the predictive accuracy and clinical applicability. Results: From a total of 12 factors, a scoring model was constructed from the three most prominent factors—ultrasound findings showing no surrounding endometrium, myometrial thinning of less than 5 mm, and vaginal bleeding—all of which demonstrated high feature importance. This predictive score identified IP with a negative predictive value of 0.950 in the low-risk group and a positive predictive value of 1.000 in the high-risk group, whereas the overall area under the curve was 0.998 (95% confidence interval, 0.992–1.000). Conclusions: The statistically derived predictive model––ultrasound showing no surrounding endometrium and myometrial thinning < 5 mm combined with vaginal bleeding––demonstrated high accuracy and practical applicability for IP diagnosis, providing a robust tool to enhance clinical decision-making and optimize routine management strategies for IP.

Jung YJ, et al. J Korean Med Sci. 2025 Oct;40:e302. https://doi.org/10.3346/jkms.2025.40.e302

Maternal hyperglycemia, induced by gestational diabetes mellitus (GDM), has detrimental effects on fetal vascular development, ultimately increasing the risk of cardiovascular diseases in offspring. The potential underlying mechanisms through which these complications occur are due to functional impairment and epigenetic changes in fetal endothelial progenitor cells (EPCs), which remain less defined. We confirm that intrauterine hyperglycemia leads to the impaired angiogenic function of fetal EPCs, as observed through functional assays of outgrowth endothelial cells (OECs) derived from fetal EPCs of GDM pregnancies (GDM-EPCs). Notably, PCDH10 expression is increased in OECs derived from GDM-EPCs, which is associated with the inhibition of angiogenic function in fetal EPCs. Additionally, increased PCDH10 expression is correlated with the hypomethylation of the PCDH10 promoter. Our findings demonstrate that in utero exposure to GDM can induce angiogenic dysfunction in fetal EPCs through altered gene expression and epigenetic changes, consequently increasing the susceptibility to cardiovascular diseases in the offspring of GDM mothers.

Maternal hyperglycemia, induced by gestational diabetes mellitus (GDM), has detrimental effects on fetal vascular development, ultimately increasing the risk of cardiovascular diseases in offspring. The potential underlying mechanisms by which these complications occur are through functional impairment and epigenetic changes in fetal endothelial progenitor cells (EPCs), however, remain less defined. We confirm that intrauterine hyperglycemia leads to impaired angiogenic function of fetal EPCs, as observed through functional assays of outgrowth endothelial cells (OECs) derived from fetal EPCs of GDM pregnancies (GDM-EPCs). Notably, PCDH10 expression is increased in OECs derived from GDM-EPCs, which is associated with the inhibition of angiogenic function in fetal EPCs. Additionally, increased PCDH10 expression is correlated with hypomethylation of the PCDH10 promoter. Our findings demonstrate that in utero exposure to GDM can induce angiogenic dysfunction in fetal EPCs through altered gene expression and epigenetic changes, consequently increasing the susceptibility to cardiovascular diseases in offspring of GDM mothers.