Increased serum strontium levels and altered oxidative stress status in early-onset preeclampsia

Background: Correctly distinguishing preeclampsia (PE), gestational hypertension (GH), and intrauterine growth retardation (IUGR) is a challenge for clinicians due to existing similarities. In our previous study, we showed that serum strontium (Sr) levels were elevated in preeclamptic women compared to healthy and GH pregnant women at the end of pregnancy. The main aim of this study was to evaluate Sr and oxidative stress in PE at the time of symptoms onset and before and compare it with IUGR/GH. Methods: Samples collected at symptoms onset included 77 preeclamptic women and 72 women diagnosed with IUGR/GH divided into two groups according to the gestational extraction week (< 34 and >= 34). Fifteen patients were also serialized until delivery. Samples collected before symptoms onset included 140 women who developed early-onset PE (E-PE, n=9), late-onset PE (L-PE, n=13), IUGR (n=9), GH (n=32) and no pathologies (n=77). Strontium, placental growth factor (PlGF), soluble fms-like tyrosine kinase 1 (sFlt-1), uric acid (UA), creatinine, lipid peroxidation, and total antioxidant activity (TAA) were measured. Results: Mean Sr, sFlt-1/PIGF ratio, UA, and lipid peroxidation/TAA ratio levels were significantly higher (p=0.002,< 0.0001,< 0.0001 and=0.03, respectively) and estimated glomerular filtration rate (eGFR) and TAA significantly lower (p=0.0008 and < 0.0001, respectively) in E-PE vs other pathologies when gestational extraction week was < 34. There was a significant correlation between Sr and eGFR (r=0.43, p=0.02), sFlt-1/PIGF ratio (r=0.56, p=0.002), TAA and gestational week of sampling (r=-0.45, p=0.02) and UA (r=-0.82, p < 0.0001) in the E-PE serial samples. No differences were found in Sr levels before symptoms onset. Conclusion: Serum Sr concentration and oxidative status are increased in E-PE when compared to other pathologies at the time of symptoms onset. More studies are needed to elucidate the causes of Sr levels elevation and its role in the pathophysiology of PE.