Is the atherosclerotic phenotype of preeclamptic placentas due to altered lipoprotein concentrations and placental lipoprotein receptors? Role of a small-for-gestational-age phenotype.

Atherosis of spiral arteries in uteroplacental beds from preeclamptic women resemble those of atherosclerosis, characterized by increased plasma lipids and lipoproteins. We hypothesized that: 1) lipoprotein receptors/transporters in the placenta would be upregulated in preeclampsia, associated with increased maternal and fetal lipoprotein concentrations; and 2) expression of these would be reduced in preeclamptic placentae from women delivering small-for-gestational-age (SGA) infants. Placental biopsies and maternal and umbilical serum samples were taken from 27 normotensive and 24 preeclamptic women. Maternal/umbilical cord serum LDL, HDL, total cholesterol, and triglycerides were measured. Placental mRNA expression of lipoprotein receptors/transporters were quantified using quantitative RT-PCR. Protein localization/expression of LDL receptor-related protein 1 (LRP-1) in the preeclamptic placentae with/without SGA was measured by immunohistochemistry. Placental mRNA expression of all genes except paraoxonase-1 (PON-1), microsomal triglyceride transfer protein (MTTP), and protein disulfide isomerase family A member 2 (PDIA2) were observed. No differences for any lipoprotein receptors/transporters were found between groups; however, in the preeclamptic group placental LRP-1 expression was lower in SGA delivering mothers (n = 7; P = 0.036). LRP-1 protein was localized around fetal vessels and Hofbauer cells. This is the first detailed study of maternal/fetal lipoprotein concentrations and placental lipoprotein receptor mRNA expression in normotensive and preeclamptic pregnancies. These findings do not support a role of altered lipid metabolism in preeclampsia, but may be involved in fetal growth.

Nutritional status evaluated by multi-frequency bioimpedance is not associated with quality of life or depressive symptoms in hemodialysis patients.

Hemodialysis therapy significantly impacts on patients' physical, psychological, and social performances. Such reduced quality of life depends on several factors, such as malnutrition, depression, and metabolic derangements. This study aims to evaluate the current nutritional status, quality of life and depressive symptoms, and determine the possible relationships with other risk factors for poor outcomes, in stable hemodialysis patients. This was a single-center, cross-sectional study that enrolled 59 adult patients undergoing hemodialysis. Laboratory tests that included high-sensitivity c-reactive protein (CRP), and quality of life and depressive symptom evaluation, as well as malnutrition-inflammation score, nutritional status and body composition (by direct segmental multi-frequency bioimpedance analysis) determinations were performed. Patients were classified as "underfat", "standard", "overfat", or "obese" by multi-frequency bioimpedance analysis. Seven patients were underfat, 19 standard, 19 overfat, and 14 obese. Triglyceride levels significantly differed between the underfat, standard, overfat, and obese groups (1.06 [0.98-1.98]; 1.47 [1.16-1.67]; 2.53 [1.17-3.13]; 2.12 [1.41-2.95] mmol/L, respectively; P=0.026), as did Kt/V between the underfat, overfat, and obese groups (1.49 ± 0.14; 1.23 ± 0.19; 1.19 ± 0.22; P=0.015 and P=0.006, respectively). Depressive symptoms, quality of life, and CRP and phosphate levels did not diverge among nutritional groups. Creatinine, albumin, and phosphate strongly correlated, as well as percent body fat, body mass index, and waist circumference (r=0.859 [P<0.001], and r=0.716 [P<0.001], respectively). Depressive symptoms and physical and psychological quality-of-life domains also strongly correlated (r(s) = -0.501 [P<0.001], r(s) = -0.597 [P<0.001], respectively). The majority of patients were overfat or obese and very few underfat. Inflammation was prevalent, overall. No association of nutritional status with malnutrition-inflammation, quality of life, or depressive symptoms could be established.

Angiotensin-converting enzyme gene polymorphism in preeclampsia and normal pregnancy.

OBJECTIVE: The purpose of this study was to evaluate the angiotensin-converting enzyme gene polymorphism in pregnant women with and without preeclampsia. STUDY DESIGN: Preeclampsia was defined as hypertension and pathologic proteinuria in pregnant women after gestational week 20. Genomic DNA was isolated from leukocytes. The insertion-deletion polymorphism in intron 16 of the angiotensin-converting enzyme gene was detected in DNA samples with the use of the polymerase chain reaction. Chi-squared and Student t tests were used for statistical analysis. RESULTS: In preeclampsia (n=51 women) angiotensin-converting enzyme genotypes were deletion-D (DD) in 16 women (31%), insertion-I (II) in 12 women (24%), and insertion-deletion in 23 women (45%); in the control group (n=71), the angiotensin-converting enzyme genotypes were DD in 21 women (30%), II in 17 women (24%), and insertion-deletion in 33 women (46%). Angiotensin-converting enzyme genotype distribution and allelic frequencies were not different between groups. CONCLUSION: No difference in the angiotensin-converting enzyme genotype distribution was found between preeclampsia and normal pregnancy. The results showed no association between angiotensin-converting enzyme polymorphism and the development of preeclampsia.