Preeclampsia is a common pregnancy-specific disease in China. With the deepening of research, clinicians have gradually realized that it is not only a major cause of adverse outcomes for both pregnant women and fetuses, but also an independent risk factor for long-term cardiovascular diseases in women. By inducing cardiac structural and functional changes, it primarily increases the risk of long-term cardiovascular diseases, including atherosclerosis, coronary artery disease, and heart failure. In future clinical practice, it is essential to establish a lifelong risk management system across specialties for women with a history of preeclampsia, and to conduct in-depth studies on genetic/epigenetic mechanisms to develop targeted preventive strategies, thereby reducing the burden of long-term cardiovascular diseases.

Long-term maternal renal injury following severe postpartum hemorrhage is predominantly secondary to acute kidney injury (AKI) during the perinatal period. Common causes of AKI due to postpartum hemorrhage include acute tubular necrosis, acute renal cortical necrosis, disseminated intravascular coagulation, and complement-mediated thrombotic microangiopathy. This article reviews the acute renal impairment associated with severe postpartum hemorrhage and its long-term effects on materal renal function.

Preeclampsia is a pregnancy-specific syndrome that affects multiple organs of pregnant women. Renal impairment is the most common clinical complication in preeclampsia patients, and the damage to renal function further accelerates the development of preeclampsia. Therefore, monitoring and re-understanding the renal function of preeclampsia patients constitude a crucial component of its lifelong management. This article discusses the mechanisms of renal damage in preeclampsia, the incidence of long-term renal insufficiency, predictive indicators, postpartum follow-up plans, and guidance for subsequent pregnancies, aiming to provide references for clinicians in monitoring and long-term management of renal function in preeclampsia patients.

Preeclampsia is a pregnancy-specific complication characterized by new-onset hypertension after 20 weeks of gestation with multi-organ injury. It can adversely affect adaptive developmental changes in offspring through epigenetic modifications, thereby increasing their risk of multi-systemic disorders. Notably, the detrimental effects on offspring vary depending on the gestational age at delivery and the severity of preeclampsia. This article reviews the impacts of preeclampsia on offspring.

Gestational diabetes mellitus (GDM) exerts multidimensional and life-course impacts on maternal and offspring health. For the mother, GDM serves as a strong predictor for future development of type 2 diabetes, metabolic syndrome, and cardiovascular diseases. For the offspring, the intrauterine hyperglycemic environment increases the risks of obesity and insulin resistance from childhood to adulthood, and may also adversely affect neuropsychiatric development. This review emphasizes GDM as a critical " window-period disease" and prioritizes its long-term consequences for both mothers and children. It calls for implementing precision antenatal management during pregnancy, establishing structured postpartum surveillance systems, and promoting personalized lifestyle interventions. These coordinated approaches are imperative for mitigating long-term disease risks across generations.

To analyze the relationship between blood loss volume and the etiologies as well as risk factors of severe postpartum hemorrhage (sPPH), providing a basis for developing and optimizing targeted preventive measures.

A retrospective study was conducted on clinical data from 683 patients with sPPH admitted to Shenzhen Maternity and Child Healthcare Hospital between January 2018 and December 2022. Patients were stratified into three groups based on blood loss volume: Group A (1 000~1 499 ml, n=385), Group B (1 500~2 499 ml, n=183), and Group C (≥2 500 ml, n=115). The causes of sPPH, relevant prenatal and intrapartum factors, multivariate analysis, and adverse pregnancy outcomes were analyzed.

Among the 683 sPPH cases, the etiologies were uterine atony (7.91%, 54/683), placental factors (38.51%, 263/683), birth canal laceration (5.42%, 37/683), and coagulopathy (4.25%, 29/683). Group A: 255 cases (66.23%) of uterine atony and 99 cases (25.71%) of placental factors; Group B: 81 cases (44.26%) of uterine atony and 81 cases (44.26%) of placental factors; Group C: 18 cases (15.65%) of uterine atony and 83 cases (72.17%) of placental factors. The differences in the distribution of both uterine atony and placental factors among the groups were statistically significant ( χ²=96.478 and 84.216, respectively; both P<0.001). Univariate analysis identified 15 factors associated with the severity of sPPH: maternal age ≥40 years, gestational age, primigravida, multiparity, history of intrauterine procedures, previous cesarean delivery(≥1), conception via assisted reproductive technology(ART), placenta accreta, placenta previa, pregnancy with uterine scar, cesarean delivery, and pre-delivery levels of hemoglobin, fibrinogen, serum calcium, and creatinine. Logistic regression revealed four independent factors for sPPH: placenta accreta (OR=4.386, 95%CI: 2.765~6.956, P<0.001), number of previous cesarean deliveries (OR=1.441, 95%CI: 1.016-2.043, P<0.05), ART conception (OR=1.512, 95%CI: 1.047~2.183, P<0.05), and pre-delivery fibrinogen level (OR=0.811, 95%CI: 0.659~0.998, P<0.05). As blood loss increased, the rates of blood transfusion (52.47%, 90.71%, 100.00%; χ²=144.865), ICU admission (18.44%, 54.64%, 93.04%; χ²=387.123), hemorrhagic shock (0.52%, 4.37%, 10.43%; χ²=28.988), and hysterectomy (0.26%, 0, 13.91%; χ²=74.392) showed a significant upward trend (all P<0.001).

Uterine atony was the primary cause of sPPH, but the proportion of placental factors increased with greater blood loss. Placenta accreta, number of previous cesarean deliveries, and ART conception were independent risk factors for sPPH, while pre-delivery fibrinogen level served as a protective factor. Early recognition, diagnosis, intervention, and comprehensive management are essential to improve maternal outcomes.