Preeclampsia(PE), a prevalent pregnancy complication, frequently poses severe implications for both pregnant women and fetuses, and its occurrence is currently exhibiting a marked upward trend[8].The fundamental pathological and physiological alterations associated with PE involve systemic small vessel spasms and endothelial injury, stemming from a complex interplay of various factors, mechanisms, and pathways[9]. Despite extensive research, the precise etiology and pathogenesis of PE remain incompletely understood to this day[10].
Extensive research indicates that PE can inflict damage on numerous organs, encompassing the brain, kidneys, liver, cardiovascular system, blood system, uterus, and placenta[11]. Notably, kidney damage often manifests in the early stages of PE, which could be promptly identified through laboratory testing, commonly characterized by the presence of urinary protein and abnormal serological markers[12].The precise mechanism underlying renal injury in PE remains elusive. Prior investigations have illuminated the key pathological and physiological alterations, including damage to glomerular endothelial cells, disruption of the interaction between endothelial cells and podocytes, basement membrane thickening, and mesangial cell proliferation[13]. These changes are potentially linked to inadequate placental perfusion in PE, which triggers the release of significant amounts of placental factors that compromise the function of endothelial cells and podocytes[14]. Furthermore, immune dysregulation and deposition of immunoreactive substances may contribute to endothelial and basement membrane damage[15].Previous research has demonstrated that an elevation of UA among PE patients could manifest during the 24-25th week of pregnancy or even prior[16]. A study conducted by Wolak Talya et al. examined the UA levels of 5507 pregnant women within the first 20 weeks of gestation[17].Their findings revealed that UA was served as an independent risk factor for PE,and individuals with UA levels exceeding the 75th percentile of the normal range were at a heightened risk of developing this condition.
Previous studies indicated a potential correlation between abnormal serum lipid metabolism and the likelihood of PE[18]. Specifically, when compared to healthy pregnant women, those diagnosed with PE exhibited significantly elevated levels of serum TG, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), and very low-density lipoprotein (VLDL).Previous studies have revealed that abnormal lipid metabolism might be implicated in the pathogenesis of PE, encompassing diminished fatty acid oxidation capacity in the placenta[19], endothelial damage stemming from elevated levels of free fatty acids[20], potentiation of microcirculation coagulation function by lipoprotein-a[21], enhanced triglyceride synthesis, and the accumulation of triglyceride-rich lipoproteins[22].However, the precise underlying mechanism remains poorly elucidated in existing literature.According to the study conducted by Ray et al., after adjusting for confounding variables like age, BMI, and parity, the data revealed that women with elevated triglyceride levels exhibited a fourfold higher risk of developing PE compared to those with normal triglyceride levels[23].
In this study, both univariate and multivariate analyses revealed a distinct elevation in renal function markers and blood lipid levels, particularly TG, Cr, and UA, among the PE group compared to the control group. This significant increase suggested that these three factors might serve as independent risk indicators for PE, aligning with previous research findings[24, 25].ROC curves indicated that UA possessed the most substantial AUC among TG, Cr, and UA. Remarkably, the joint of TG, Cr, and UA yielded an even larger AUC surpassing UA alone in predicting PE while maintaining satisfactory specificity and sensitivity.This signified that the joint of TG,Cr and UA held significant predictive value for the occurrence of PE.
However, this study was retrospective and thus inherently bore limitations, including potential selection bias and incomplete data collection. For instance, individuals who terminated pregnancy before 28 weeks owing to the severity of the illness or those who failed to provide fasting blood samples during late pregnancy due to the rapid disease progression were excluded from this study. Additionally, the relatively small sample size is also a consideration. Therefore, the findings of this research need to be further validated through larger, multi-center, prospective studies with a larger sample size.