Prediction of pre-eclampsia combining NGAL and other biochemical markers with Doppler in the first and/or second trimester of pregnancy. A pilot study.

Karampas, Grigorios; Eleftheriades, Makarios; Panoulis, Konstantinos; Rizou, Myrto; Haliassos, Alexander; Metallinou, Dimitra; Mastorakos, George; Rizos, Demetrios

doi:10.1016/j.ejogrb.2016.08.034

Cited by 21 publications

(26 citation statements)

References 40 publications

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“…Given our interest in iron, it is not surprising that it is changed during PE. While one study suggested it to be decreased in PE (827), a great many other studies showed it to be increased significantly in PE, and typically in a manner that correlated with PE severity (735, 828–837). Pertinently to PE, it is also well established as an early biomarker of acute kidney injury (AKI) (838–841).…”

Section: Proteomic and Similar Biomarkers – Circulating And Placentalmentioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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Preeclampsia (PE) is a complex, multisystem disorder that remains a leading cause of morbidity and mortality in pregnancy. Four main classes of dysregulation accompany PE and are widely considered to contribute to its severity. These are abnormal trophoblast invasion of the placenta, anti-angiogenic responses, oxidative stress, and inflammation. What is lacking, however, is an explanation of how these themselves are caused. We here develop the unifying idea, and the considerable evidence for it, that the originating cause of PE (and of the four classes of dysregulation) is, in fact, microbial infection, that most such microbes are dormant and hence resist detection by conventional (replication-dependent) microbiology, and that by occasional resuscitation and growth it is they that are responsible for all the observable sequelae, including the continuing, chronic inflammation. In particular, bacterial products such as lipopolysaccharide (LPS), also known as endotoxin, are well known as highly inflammagenic and stimulate an innate (and possibly trained) immune response that exacerbates the inflammation further. The known need of microbes for free iron can explain the iron dysregulation that accompanies PE. We describe the main routes of infection (gut, oral, and urinary tract infection) and the regularly observed presence of microbes in placental and other tissues in PE. Every known proteomic biomarker of “preeclampsia” that we assessed has, in fact, also been shown to be raised in response to infection. An infectious component to PE fulfills the Bradford Hill criteria for ascribing a disease to an environmental cause and suggests a number of treatments, some of which have, in fact, been shown to be successful. PE was classically referred to as endotoxemia or toxemia of pregnancy, and it is ironic that it seems that LPS and other microbial endotoxins really are involved. Overall, the recognition of an infectious component in the etiology of PE mirrors that for ulcers and other diseases that were previously considered to lack one.

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Section: Proteomic and Similar Biomarkers – Circulating And Placentalmentioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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“…Many of the studies were excluded after full-text review because the circulating ADMA was measured after the diagnosis of preeclampsia. Because three [ 15 , 16 , 18 ] of the include studies reported two sets of circulating ADMA data based on different GA of sampling, eleven comparisons were available for the different of circulating ADMA before the onset of preeclampsia. Only two studies [ 16 , 17 ] reported data regarding the predictive efficacy of circulating ADMA for the incident risk of preeclampsia.…”

Section: Resultsmentioning

confidence: 99%

“…The characteristics of included studies were shown in Table 1 . All of the included studies recruited women with apparent normal pregnancies at the enrollment, and seven of them included women with singleton pregnancies only [ 14 , 15 , 17 – 19 , 21 ]. The sample size of the included pregnant women varied from 44 to 375, and the GA of sampling for the measurement of circulating ADMA were from 6 to 25 weeks.…”

Section: Resultsmentioning

confidence: 99%

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Circulating asymmetric dimethylarginine and the risk of preeclampsia: a meta-analysis based on 1338 participants

et al. 2017

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BackgroundPatients with preeclampsia have higher circulating asymmetric dimethylarginine (ADMA). However, whether circulating ADMA is elevated before the diagnosis of preeclampsia has not been determined.MethodsA meta-analysis of observational studies that reported circulating ADMA level before the onset of preeclampsia was performed. Pubmed and Embase were searched. Standardized mean differences (SMD) with 95% confidence intervals (CI) were used to estimate the differences in circulating ADMA. A random effect model or a fixed effect model was applied depending on the heterogeneity. The predictive efficacy of circulating ADMA for the incidence of preeclampsia was also explored.ResultsEleven comparisons with 1338 pregnant women were included. The pooled results showed that the circulating ADMA was significantly higher in women who subsequently developed preeclampsia as compared with those did not (SMD: 0.71, p < 0.001) with a moderate heterogeneity (I2 = 43%). Stratified analyses suggested elevation of circulating ADMA is more remarkable in studies with GA of ADMA sampling ≥ 20 weeks (SMD: 0.89, p < 0.01) as compared those with GA of ADMA sampling < 20 weeks (SMD: 0.56, p < 0.01; p for subgroup interaction = 0.03). Differences of maternal age, study design, and ADMA measurement methods did not significantly affect the results. Only two studies evaluated the potential predicting ability of circulating ADMA for subsequent preeclampsia, and retrieved moderate predictive efficacy.ConclusionsCirculating ADMA is elevated before the development of preeclampsia. Studies are needed to evaluate the predictive efficacy of ADMA for the incidence of preeclampsia.

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“…Similar to D'Anna et al (14), Youssef et al (17) evaluated serum NGAL levels during pregnancy and have shown that combination of the first-trimester serum NGAL measurement and uterine artery Doppler, serum PAPP-A, PIGF, P-Selectin, sFLT-1 could improve the predictive value for late-onset preeclampsia. Karampas et al (18) have shown that a combination of the first and second-trimester uterine artery pulsatility index (UtA-PI), ductus venosus pulsatility index (DV-PI) and a marker panel including PAPP-A, PIGF, sFlt-1, s-Flt-1/PIGF, ADMA, MMP-9, MMP-9/NGAL may improve the detection of preeclampsia.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil Gelatinase-Associated Lipocalin Levels in Early and Late Onset Preeclampsia

Güralp

Tüten²,

Öncül

et al. 2020

Gynecol Obstet Reprod Med

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Objective: To evaluate the serum neutrophil gelatinase-associated lipocalin levels in pregnant women with and without preeclampsia, early-onset preeclampsia and late-onset preeclampsia, preeclampsia with and without severe features, and investigate the correlation with the neonatal outcomes.Study Design: A total of 79 pregnant women, 27 with uncomplicated pregnancies, 30 with early-onset preeclampsia, and 22 with late-onset preeclampsia were evaluated in a cross-sectional study. Neutrophil gelatinase-associated lipocalin was measured with a colorimetric Sandwich-ELISA method. Age; body mass index; systolic and diastolic blood pressure; umbilical-artery Doppler results; serum urea, bilirubin, uric acid, AST, ALT; 24-hour protein test; birth-weight; and Apgar-scores were recorded. Results: Serum neutrophil gelatinase-associated lipocalin levels were significantly higher in women with preeclampsia compared to those without preeclampsia (p<0.001); in women with early-onset preeclampsia compared to those with late-onset preeclampsia (p<0.001); and in women with late-onset preeclampsia compared to those without preeclampsia (p=0.028). Mean serum neutrophil gelatinase-associated lipocalin levels were comparable in women with preeclampsia with and without severe features (p=0.076). The correlation analysis showed that neutrophil gelatinase-associated lipocalin was not affected by age or body mass index. Neutrophil gelatinase-associated lipocalin had a positive correlation with systolic and diastolic blood pressure and the umbilical-artery PI and RI. Serum neutrophil gelatinase-associated lipocalin had a positive correlation with serum urea (r=0.416, p=0.031) however had no significant correlation with birth-weight, Apgar-scores, uric acid and amount of proteinuria in women with preeclampsia. Conclusion: Serum neutrophil gelatinase-associated lipocalin levels were significantly higher in women with preeclampsia compared to those without preeclampsia; in women with early-onset preeclampsia compared to those with late-onset preeclampsia, and in women with late-onset preeclampsia compared to women without preeclampsia. Mean serum neutrophil gelatinase-associated lipocalin levels were comparable in women with preeclampsia with and without severe features.

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Prediction of pre-eclampsia combining NGAL and other biochemical markers with Doppler in the first and/or second trimester of pregnancy. A pilot study.

Cited by 21 publications

References 40 publications

A Dormant Microbial Component in the Development of Preeclampsia

A Dormant Microbial Component in the Development of Preeclampsia

Circulating asymmetric dimethylarginine and the risk of preeclampsia: a meta-analysis based on 1338 participants

Neutrophil Gelatinase-Associated Lipocalin Levels in Early and Late Onset Preeclampsia

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