Pregnancy-induced hypertension (PIH) affects 5–8 % of pregnancies [1], [2], [3] and may be complicated by preeclampsia (PE). The diagnosis of PE is complex and based on anamnesis, physical examination and a combination of laboratory and ultrasound parameters, which can delay the appropriate treatment [2]. From a clinical perspective, it would be important to identify a marker that could become a single diagnostic test for PE [4], [5].

PIH is one of the risk factors for preterm delivery which is connected with increased morbidity and mortality. Complications, such as preeclampsia and eclampsia, affect approximately 1–5 % of pregnancies. Eclampsia is an emergency condition for both mother and fetus [6]. It results in numerous complications, such as: premature separation of the placenta, bleeding, DIC or HELLP syndrome, and it prolongs the duration of maternal and neonatal hospitalization. Although PIH is diagnosed after the 20th week of gestation, the disease is considered to begin in the first trimester, at the time of placenta formation and remodeling of spiral arteries of the uterus [7], [8]. Systemic inflammatory response and dysfunction of maternal endothelial cells seem to be crucial for the pathogenesis of this disorder [3], [6]. So far, the best treatment option is the normalization of arterial blood pressure, which in turn reduces or prevents organ malfunction. So far placenta removal remains the only successful method of PIH and PE treatment [8].

Sirtuins are members of the NAD+-dependent family of protein deacetylases. They are involved in the regulation of cell proliferation, apoptosis, autophagy, inflammation and redox regulation [9], [10], [11], [12]. Sirtuin-1 (Sirt1) is a nutrient-sensor which inhibits adipogenesis, enhances fat mobilization, and its expression is reduced in PE syncytiotrophoblast [13]. Interestingly, resveratrol, an activator of SIRT-1, reverses the elevated blood pressure and proteinuria in a rat model of PE [14]. Sirtuins, expressed in human placentas, are involved in regulation of metabolic pathways [15], [16]. Sirt2 protein expression is lowered in pre-term PE placentas as compared to normal pregnancies [17]. Sirt1 expression is diminished in mice PE placentas as compared to healthy controls [18].

Leptin affects the secretion of gonadotropins, placenta formation and transmission of signals at the maternal-fetal unit level. Abnormal leptin concentration is associated with: recurrent miscarriages, intrauterine growth restriction and polycystic ovary syndrome [19], [20]. Increased number of leptin receptors and a significant increase in serum leptin concentration was shown in PE [21]. In a case-control study including a group of 74 women with preeclampsia and 79 healthy pregnant women, it was demonstrated that BMI, leptin and resistin concentrations were significantly higher in the group of women with PE. Adiponectin concentration remained at a similar level in both groups. In the statistical regression model, it was demonstrated that (i) BMI >28 kg/m2 and (ii) higher leptin concentrations are independent risk factors of PE [21]. In addition, plasma leptin concentration was positively correlated with BMI and negatively related with the birth weight of newborns [21], [22].

In contrast, it was shown in a group of 80 patients (23 with mild PE, 29 with severe PE and 28 healthy pregnant women) that leptin levels were similar in healthy pregnant women and in those with PIH and PE. In addition, the authors indicated that the concentration of leptin was not related to gestational age [23].

The number of studies on sirtuin levels in pregnant women are very limited. Thus we determined blood concentrations of sirtuin 1, 3 and 6 in women with PIH and compared their levels to healthy pregnant women. Furthermore we measured leptin and adiponectin levels in both groups.