In these females PE risk during the second pregnancy was associated with the lowest placenta weight during the first pregnancy (odds ratio (OR) 1.30, 95% CI 1.14-1.47). Authors considered that low placenta weight during the first pregnancy has been associated with higher pre-eclampsy risk during the second pregnancy. Moreover, females that had no pre-eclampsy during the first pregnancy also had higher placenta weight [11].
L.K. Proctor et al demonstrated the association between lesser umbilical cord diameter with lower placenta weight and fetus body weight at birth. Presumably, thinner umbilical cord can contribute to development of placenta failure and retarded fetus growth [12].
Siveska EJ et al (USA) reported association between inadequate fetus growth with higher PE risk. Changes of fetal development and rapid placenta degradation resulting in arterial pressure increase can be detected by scanning – the best diagnostic option of ante-natal IUGR detection. These results support the hypothesis stating that PE is a heterogeneous disorder possibly manifested by at least two types of pre-eclampsy, namely delayed fetus maturation and maturation corresponding to normal gestation terms. Delayed maturation pregnancy often results in pre-term labors, while pregnancy with normal maturation terms usually results in normal terms labors. Study results indicate that fetus size is an important PE predictor.[13]
The study by Bhattacharjee et al (2017) studied the effect of placenta location on PE development. The study enrolled 200 pregnant females, 100 study patients had lateral placenta location, another 100 patients had central placenta location. Pre-eclampsy has been reported in 66% of 100 females with lateral placenta location and in 36% of patients with central placenta. Therefore, the risk of pre-eclampsy in females with lateral placenta location was 5 fold higher compared to patients with central placenta location. [14]
Parul S. Jani studied pregnant females with lateral placenta location by color Doppler evaluation of uterine arteries resistance. 26 of 80 patients with lateral placenta location had elevated uterine arteries resistance index; 22 of them have developed pre-eclampsy. 54 pregnant females had no changes of uterine arteries resistance and only 6 of them had pre-eclampsy (р <0 001). Uterine arteries resistance evaluation sensitivity level reached 84.6%, with specificity level 88.8%, positive prognostic index level 78.5% and negative prognostic index 92.3%. Authors conclude that patients with lateral placenta location have a higher risk of pre-eclampsy; however, test sensitivity and specificity can be facilitated by evaluation of uterine arterial flow thus enabling the prediction of PE in females with lateral placenta location and higher resistance level of uterine arteries [15].
Renal disease is one of the key factors of maternal PE. It is associated with vascular tonus disorders and hypertension [16]. According to US Preventive Services Task Force (USPSTF) recommendations (2014) renal disorder is considered PE risk factor [17].
PE diagnosing in patients with chronic renal disorders is complicated due to pre-existing proteinuria. PE risk in patients with chronic renal disease is 5.3% - 8%, compared to 1.8% in healthy patients [18].
During physiological pregnancy glomerular filtration rate (GFR) increase up to 50% is reported during the second trimester resulting in lower serum creatinine level. Therefore, lower serum creatinine levels are reported during pregnancy compared to prior levels. Correspondingly, normal levels reported in non-pregnant patients (1-1.2 mg/dl) can indicate renal dysfunction when reported during pregnancy [19].
Plasma creatinine level increase is associated with creatinine tubular secretion increase that can be misinterpreted as elevated GFR in patients with moderate to severe decrease of corresponding levels (<50 ml/min). Non-linear correlation between plasma creatinine level and GFR values makes the detection of mild glomerular filtration disorders [20].