Marta Ribeiro Hentschke1, Luiza Silveira Lucas2, Hiten D Mistry3, Bartira E Pinheiro da Costa4, Carlos E Poli-de-Figueiredo5. 1. Laboratory of Nephrology, Institute of Biomedical Research, São Lucas Hospital, School of Medicine, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS, Brazil. Electronic address: martarh@yahoo.com.br. 2. Laboratory of Nephrology, Institute of Biomedical Research, São Lucas Hospital, School of Medicine, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS, Brazil. Electronic address: luizalucas@gmail.com. 3. Division of Hypertension, Department of Nephrology, Hypertension, Clinical Pharmacology and Clinical Research, University of Bern, Berne, Switzerland. Electronic address: hiten.mistry@kcl.ac.uk. 4. Laboratory of Nephrology, Institute of Biomedical Research, São Lucas Hospital, School of Medicine, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS, Brazil. Electronic address: bart@pucrs.br. 5. Laboratory of Nephrology, Institute of Biomedical Research, São Lucas Hospital, School of Medicine, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS, Brazil. Electronic address: cepolif@pucrs.br.
Abstract
INTRODUCTION: Endocan-1 has been proposed as a possible biomarker and predictor of vascular endothelial related pathologies. Thus, we hypothesised that Endocan-1 levels would be up-regulated in maternal plasma and placentae from women with pre-eclampsia. The aim of our study was to compare Endocan-1 concentrations in maternal/fetal plasma and placentae from normotensive and pre-eclamptic pregnancies. METHODS: Observational and case-controlled study, at the São Lucas Hospital, Brazil. Placental biopsies, maternal/umbilical venous (fetal) plasma were taken from 67 normotensive and 50 pre-eclamptic women. Endocan-1 levels were quantified using MagPlex(TH)-C and analysed by Analysis of Covariance and Pearson correlation. The null hypothesis was rejected at p<0.05. RESULTS: Higher levels of Endocan-1 were found in maternal plasma in the pre-eclamptic group (mean ratio=1.49; 95% confidence interval: 1.19-1.85, p=0.001), with a moderate effect size (Cohen's D=0.84). Placental Endocan-1 levels (μg/g) were lower in pre-eclampsia (1.52 [1.10, 2.40] vs. 2.24 [1.32, 3.75], p=0.033) and fetal Endocan-1 concentration (ng/ml) did not show any difference between groups (3.10 [2.60, 4.54] vs. 2.91 [2.20, 3.66] p=0.085). In addition, an up-regulation of maternal plasma Endocan-1 in the pre-eclamptic group was observed when stratified in relation to gestational age, systolic blood pressure and proteinuria (p<0.05, for all). Furthermore, a positive correlation between Endocan-1 concentration in maternal vs. fetal plasma was also found (r=0.258, p=0.015). For the matched samples, a negative correlation between Endocan-1 in maternal/fetal plasma with birthweights, placental weights and gestational age at delivery was observed (p<0.05 for all). DISCUSSION: Endocan-1 is increased in women with pre-eclampsia for all strata, which highlight the importance of this molecule as a possible biomarker. The negative correlations between Endocan-1 and clinical data suggest that this molecule may also be involved with prematurity and low birth weight, which warrants further investigations.
INTRODUCTION: Endocan-1 has been proposed as a possible biomarker and predictor of vascular endothelial related pathologies. Thus, we hypothesised that Endocan-1 levels would be up-regulated in maternal plasma and placentae from women with pre-eclampsia. The aim of our study was to compare Endocan-1 concentrations in maternal/fetal plasma and placentae from normotensive and pre-eclamptic pregnancies. METHODS: Observational and case-controlled study, at the São Lucas Hospital, Brazil. Placental biopsies, maternal/umbilical venous (fetal) plasma were taken from 67 normotensive and 50 pre-eclamptic women. Endocan-1 levels were quantified using MagPlex(TH)-C and analysed by Analysis of Covariance and Pearson correlation. The null hypothesis was rejected at p<0.05. RESULTS: Higher levels of Endocan-1 were found in maternal plasma in the pre-eclamptic group (mean ratio=1.49; 95% confidence interval: 1.19-1.85, p=0.001), with a moderate effect size (Cohen's D=0.84). Placental Endocan-1 levels (μg/g) were lower in pre-eclampsia (1.52 [1.10, 2.40] vs. 2.24 [1.32, 3.75], p=0.033) and fetal Endocan-1 concentration (ng/ml) did not show any difference between groups (3.10 [2.60, 4.54] vs. 2.91 [2.20, 3.66] p=0.085). In addition, an up-regulation of maternal plasma Endocan-1 in the pre-eclamptic group was observed when stratified in relation to gestational age, systolic blood pressure and proteinuria (p<0.05, for all). Furthermore, a positive correlation between Endocan-1 concentration in maternal vs. fetal plasma was also found (r=0.258, p=0.015). For the matched samples, a negative correlation between Endocan-1 in maternal/fetal plasma with birthweights, placental weights and gestational age at delivery was observed (p<0.05 for all). DISCUSSION: Endocan-1 is increased in women with pre-eclampsia for all strata, which highlight the importance of this molecule as a possible biomarker. The negative correlations between Endocan-1 and clinical data suggest that this molecule may also be involved with prematurity and low birth weight, which warrants further investigations.
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