306. PREDICTING GESTATIONAL DIABETES FROM MATERNAL ANGIOTENSIN II AND ANGIOTENSIN 1–7 LEVELS AT 15 WEEKS GESTATION

2010 ◽  
Vol 22 (9) ◽  
pp. 106
Author(s):  
S. D. Sykes ◽  
E. R. Lumbers ◽  
K. G. Pringle ◽  
T. Zakar ◽  
G. A. Dekker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Gestational Diabetes ◽  
Area Under The Curve ◽  
Renin Angiotensin System ◽  
Late Pregnancy ◽  
Early Gestation ◽  
Disease Marker ◽  
Increased Risk ◽  
Unit Increase ◽  
Plasma Angiotensin

Gestational diabetes (GD), a pregnancy complication defined by glucose intolerance with onset during pregnancy, is a condition affecting 5.5%–8.8% of Australian pregnancies1. Untreated GD increases perinatal mortality and babies from GD pregnancies have an increased risk of diabetes and obesity, whilst mothers have an increased risk of type II diabetes later in life1. Circulating levels of angiotensin 1–7 (Ang1–7), a peptide of the renin angiotensin system, have been reported to be reduced in third trimester pregnancies with GD2. The effects of Ang1–7 generally oppose those of angiotensin II (AngII) and it is possible that in early gestation pro-angiogenic functions of AngII are counterbalanced by Ang1–7, causing placental insufficiency and pregnancy complications. We wanted to determine the predictive capability of AngII and Ang1–7, in early gestation, for GD. Healthy nulliparous pregnant women from the Adelaide SCOPE cohort with GD (n = 36) or serving as controls (n = 131) had both peptides measured at 15 weeks using an RIA (D. Casley, Prosearch Pty. Ltd.) on EDTA treated plasma. A predictive model was constructed using logistic regression and area under the curve after ROC analysis (AROC, Table 1). AngII did not change the model and was omitted. This model shows that for every one unit increase of Log (Ang1–7 pg/mL) peptide levels the odds of acquiring GD increase five times, suggesting that Ang1–7 levels in early gestation may be a better disease marker than those seen at late pregnancy. (1) Hoffman L, Nolan C, Wilson JD, et al., 1998. Gestational diabetes mellitus – management guidelines. The Australasian Diabetes in Pregnancy Society. Med. J. Aust. 169, 93–97.(2) Nogueira AI, Santos RAS, Simoes e Silva AC, et al., 2007. The pregnancy-induced increase of plasma angiotensin-(1–7) is blunted in gestational diabetes. Regul. Pep., 141, 55–60.

161. PREDICTING GESTATIONAL HYPERTENSION AND PREECLAMPSIA FROM MATERNAL ANGIOTENSIN II AND ANGIOTENSIN 1–7 LEVELS AT 15 WEEKS GESTATION

2010 ◽  
Vol 22 (9) ◽  
pp. 79
Author(s):  
S. D. Sykes ◽  
E. R. Lumbers ◽  
K. G. Pringle ◽  
T. Zakar ◽  
G. A. Dekker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Gestational Hypertension ◽  
Area Under The Curve ◽  
Renin Angiotensin System ◽  
Maternal Plasma ◽  
Late Gestation ◽  
Early Gestation ◽  
Predictive Strength ◽  
Hypertensive Diseases ◽  
First Time

Angiotensin II (AngII) is the main effector peptide of the renin angiotensin system (RAS). The RAS is also involved in the aetiology of hypertension. Angiotensin 1–7 (Ang1–7) acting on the Mas receptor may counteract AngII effects. RAS activity is increased in early gestation. We wanted to determine if maternal plasma AngII and Ang1–7 levels in early gestation predict the onset of hypertension in late gestation. Circulating AngII and Ang1–7 have been measured by RIA (D Casley, Prosearch Pty. Ltd.) in EDTA treated plasma from healthy nulliparous pregnant women at 15 weeks gestation from the Adelaide SCOPE cohort for preeclampsia (PE) (n = 50) and gestational hypertension (GHT) (n = 50), with 131 controls. Log transformation and linear regression showed an inverse, weak (R2 = 0.068), statistically significant relationship (P = 0.003) between AngII and Ang1–7. The predictive capability of these peptides for pregnancy outcome was determined by logistic regression and area under the curve after ROC analysis (AROC). The summaries of these analyses are shown in Table 1. AngII did not increase the predictive strength of either model and was omitted. These models show for the first time that circulating Ang1–7 levels are highly statistically significant predictors of hypertensive diseases of pregnancy as early as 15 weeks gestation, well before diagnosis of disease.

scholarly journals Association of angiotensin II type 1-receptor gene polymorphisms with the risk of developing hypertension in Mexican individuals

2011 ◽  
Vol 13 (1) ◽  
pp. 133-140 ◽  
Author(s):  
Nancy Martínez-Rodríguez ◽  
Carlos Posadas-Romero ◽  
Guillermo Cardoso ◽  
José Manuel Pérez-Rodríguez ◽  
Nonanzit Pérez-Hernández ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Gene Polymorphisms ◽  
Complex Disease ◽  
Receptor Gene ◽  
Renin Angiotensin System ◽  
Similar Distribution ◽  
Increased Risk ◽  
Receptor Gene Polymorphisms ◽  
Genetic And Environmental Factors

Introduction: Hypertension is a complex disease in which a significant interaction between genetic and environmental factors takes place. The renin–angiotensin system plays an important role regulating blood pressure to maintain homeostasis and vascular tone. In the present work, the role of angiotensin II type 1-receptor (AGTR1) gene polymorphisms as susceptibility markers for hypertension was evaluated. Materials and methods: Five polymorphisms in the AGTR1 gene were genotyped by 5′ exonuclease TaqMan genotyping assays in 239 hypertensive and 371 non-hypertensive individuals. Results: A similar distribution of rs275651, rs275652, rs275653, and rs5183 polymorphisms was observed in both studied groups. Different distribution of rs5182 genotypes was observed between the studied groups ( p = 0.016). According to the co-dominant model, individuals with rs5182 CC genotype have a 1.83-fold increased risk of developing hypertension ( p = 0.009). Polymorphisms were distributed in two blocks: block 1 included the rs275651, rs275652, and rs275653 polymorphisms, whereas block 2 included the rs5183 and rs5182 polymorphisms. Individuals with hypertension showed increased frequency of ‘ CA’ haplotype of block 2 when compared to non-hypertensive individuals ( p = 0.015, odds ratio = 1.33). Conclusion: The results suggest that the rs5182 gene polymorphism could be involved in the risk of developing hypertension in Mexican individuals.

Longitudinal study of platelet angiotensin II binding in human pregnancy

1992 ◽  
Vol 82 (4) ◽  
pp. 377-381 ◽  
Author(s):  
Philip N. Baker ◽  
Fiona Broughton Pipkin ◽  
E. Malcolm Symonds
Keyword(s):  
Longitudinal Study ◽  
Angiotensin Ii ◽  
Post Partum ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Significant Rise ◽  
Renin Substrate ◽  
Plasma Renin Concentration ◽  
Plasma Angiotensin ◽  
In Pregnancy

1. Platelet angiotensin II binding, circulating angiotensin II levels, plasma renin substrate and plasma renin concentration were measured in a longitudinal study of 30 women during pregnancy and the puerperium. 2. There was a significant fall in platelet angiotensin II binding from 11 weeks gestation to 18 weeks gestation (P < 0.01). There were no further significant changes in platelet angiotensin II binding until after delivery, a significant rise in platelet angiotensin II binding being found at 6 weeks post partum as compared with at 36 weeks gestation (P < 0.01). There was no further significant change from 6 to 12 weeks post partum, and platelet angiotensin II binding at 6 and 12 weeks post partum in the pregnant cohort approximated to that in non-pregnant women. These changes parallel those known to occur in pressor responsiveness to angiotensin II in pregnancy. 3. Plasma angiotensin II concentration, plasma renin substrate and plasma renin concentration were all significantly higher during pregnancy than in the puerperium (P < 0.001). There were no significant changes during pregnancy in plasma angiotensin II concentration or plasma renin concentration, although plasma renin substrate rose throughout. 4. Significant inverse correlations between platelet angiotensin II binding and plasma angiotensin II concentration (P < 0.01), plasma renin substrate (P < 0.01) and plasma renin concentration (P 0>001) were found during pregnancy. These data suggest that down-regulation of platelet angiotensin II binding by the components of the renin-angiotensin system pertains in pregnancy. 5. We are currently investigating parallelism between platelet and vascular angiotensin-binding sites. If such is confirmed, studies of platelet angiotensin II binding in pregnancy may be of both basic physiological and clinical interest in relation to the hypertensive diseases of pregnancy.

scholarly journals Early prediction of gestational diabetes mellitus in the Chinese population via advanced machine learning

2020 ◽  
Author(s):  
Yan-Ting Wu ◽  
Chen-Jie Zhang ◽  
Ben Willem Mol ◽  
Andrew Kawai ◽  
Cheng Li ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Machine Learning ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Chinese Population ◽  
Feature Selection Method ◽  
Area Under The Curve ◽  
First Trimester ◽  
Record System ◽  
Increased Risk

Abstract Context Accurate methods for early gestational diabetes mellitus (GDM) (during the first trimester of pregnancy) prediction in Chinese and other populations are lacking. Objectives Establishing effective models to predict early GDM. Setting Pregnancy data for 73 variables during the first trimester were extracted from the electronic medical record system. Main measures Based on a machine learning (ML) driven feature selection method, 17 variables were selected for early GDM prediction. In order to facilitate clinical application, 7 variables were selected from the 17-variable panel. Advanced ML approaches were then employed using the 7-variable dataset and the 73-variable dataset to build models predicting early GDM for different situations respectively. Results 16,819 and 14,992 cases were included in the training and testing sets, respectively. Using 73 variables, the deep neural network model achieved high discriminative power, with area under the curve (AUC) values of 0.80. The 7-variable logistic regression (LR) model also achieved effective discriminate power (AUC = 0.77). Low BMI (≤ 17) was related to an increased risk of GDM, compared to a BMI in the range of 17 to 18 (minimum risk interval) (11.8% vs 8.7%, P = 0.0935). TT3 and TT4 were superior to FT3 and FT4 in predicting GDM. Lipoprotein (a) was demonstrated a promising predictive value (AUC = 0.66). Conclusions We employed ML models that achieved high accuracy in predicting GDM in early pregnancy. A clinically cost-effective 7-variable LR model was simultaneously developed. The relationship of GDM with thyroxine and BMI was investigated in the Chinese population.

scholarly journals Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy

1999 ◽  
Vol 160 (1) ◽  
pp. 43-47 ◽  
Author(s):  
H Kobori ◽  
A Ichihara ◽  
Y Miyashita ◽  
M Hayashi ◽  
T Saruta
Keyword(s):  
Angiotensin Ii ◽  
Thyroid Hormone ◽  
Cardiac Hypertrophy ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin ◽  
Renin Mrna

We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin-angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague-Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily i.p. injection of thyroxine (0.1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri-iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0.12+/-0.03 and 0.15+/-0.03 microgram/h per liter, 126+/-5 and 130+/-5 ng/l respectively) (means+/-s.e.m.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5.0+/-0.5 vs 3.5+/-0.1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74+/-2 vs 48+/-2%, 6.5+/-0.8 vs 3.8+/-0.4 ng/h per g, 231+/-30 vs 149+/-2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.

Renin–Angiotensin System in Mild Essential Hypertension. the Functional Significance of Angiotensin II in Untreated and Thiazide-Treated Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 319s-321s ◽  
Author(s):  
H. Ibsen ◽  
A. Leth ◽  
H. Hollnagel ◽  
A. M. Kappelgaard ◽  
M. Damkjaer Nielsen ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Functional Significance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Twenty-five patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. 2. Basal and post-frusemide values for plasma renin concentration and plasma angiotensin II concentration did not differ markedly from reference values in 25 40-year-old control subjects. In the untreated, sodium replete state saralasin infusion (5·4 nmol min−1 kg−1) produced an increase in mean arterial pressure in the patient group as a whole. 3. Twenty-one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months. Pre-treatment, frusemide-stimulated plasma renin concentration and plasma angiotensin II, and values during thiazide treatment were higher in ‘non-responders’ (n = 10) to hydrochlorothiazide treatment than in ‘thiazide-responders’ (n = 11). During thiazide therapy, angiotensin II blockade induced a clear-cut decrease in mean arterial pressure in all ‘thiazide-nonresponders’ whereas only four out of 11 ‘thiazide-responders’ showed a borderline decline in mean arterial pressure. 4. The functional significance of the renin—angiotensin system in mild essential hypertension emerges only after thiazide treatment. Thiazide-induced stimulation of the renin—angiotensin system counter-balanced the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of the renin—angiotensin system determined the blood pressure response to thiazide treatment.

scholarly journals Association between maternal serum lipids during late pregnancy and adverse birth outcomes

2020 ◽  
Author(s):  
Meng-Yi Dai ◽  
Lu-Lin Wang ◽  
Yun-Tao Wu ◽  
Huan Li ◽  
Jian-Hong Xia ◽  
...  
Keyword(s):  
Birth Outcomes ◽  
Linear Trend ◽  
Late Pregnancy ◽  
Blood Lipid ◽  
Maternal Blood ◽  
Adverse Birth Outcomes ◽  
Lipid Levels ◽  
Increased Risk ◽  
Unit Increase ◽  
Blood Lipid Levels

Abstract Background: Adverse birth outcomes have short- and long-term impacts on maternal and child health. Maternal dyslipidemia during late pregnancy has been found to be associated with increased risk of adverse birth outcomes. However, similar evidence on association between maternal blood lipid levels and adverse birth outcomes is limited in China.Methods: The data were extracted from Guangdong Women and Children Hospital Information System from September 2014 to March 2018. A total of 3951 mother-newborn pairs were included in our study. Logistic regression model and linear trend analysis were conducted to analyze the correlation between maternal blood lipid levels and adverse birth outcomes after controlling potential confounders including gestational age, pre-pregnancy body mass index, fetal sex, and parity. Results: Among the 3951 subjects, the rates of macrosomia, large-for-gestational age (LGA), low birth weight infants (LBW), and preterm birth were 3.9% (154/3951), 8.5% (334/3951), 9.5% (377/3951), and 9.8% (388/3951), respectively. LDL was a risk factor for preterm birth (OR: 1.20; 95% CI: 1.08-1.34) while HDL was a protective factor (OR: 0.73; 95% CI: 0.55-0.96) after adjusting for covariates. As every unit increase in TG, the risk of macrosomia and LGA increased by 25% (adjusted OR: 1.25; 95% CI: 1.12-1.38) and 16% (adjusted OR: 1.16; 95% CI: 1.07-1.26), respectively. However, every unit increase in HDL concentration was associated with decreased risk for LGA (adjusted OR: 0.60; 95% CI: 0.44-0.81) and macrosomia (adjusted OR: 0.64; 95% CI: 0.41-0.99). High LDL concentrations were associated with a decreased risk of macrosomia (adjusted OR: 0.82; 95% CI: 0.68-0.99) and LGA (adjusted OR: 0.86; 95% CI: 0.76-0.98) but an increased risk of LBW (adjusted OR: 1.16; 95% CI: 1.04-1.30). The results of linear trend analysis were similar to those of logistic regression model.Conclusions: Maternal dyslipidemia during the third trimester is closely related to adverse birth outcomes. Monitoring and managing maternal blood lipid levels in an appropriate range may help to reduce the burden of adverse birth outcomes.

scholarly journals Effects of L-/N-Type Calcium Channel Blockers on Angiotensin II–Renin Feedback in Hypertensive Patients

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yutaka Kawabata ◽  
Takeshi Soeki ◽  
Hiroyuki Ito ◽  
Tomomi Matsuura ◽  
Kenya Kusunose ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Calcium Channel ◽  
Renin Angiotensin System ◽  
Channel Blockers ◽  
Hypertensive Patients ◽  
Beneficial Effects ◽  
Urine Albumin ◽  
Amlodipine Group ◽  
Plasma Angiotensin ◽  
Blood Pressures

Objectives. Cilnidipine, an L-/N-type calcium channel blocker (CCB), has unique organ-protective properties due to suppression of hyperactivity in the sympathetic nervous system and renin-angiotensin system (RAS). In this study, we hypothesized that cilnidipine might exert a renoprotective effect by suppressing the RAS. Methods. A total of 25 hypertensive patients receiving a RAS inhibitor were randomly assigned to a cilnidipine (n = 12) or amlodipine (n = 13) group. The effects of cilnidipine on proteinuria and angiotensin II–renin feedback were assessed. Results. After 6 months of treatment, both systolic and diastolic blood pressures were significantly reduced to a similar extent in both groups. The urine albumin-to-creatinine ratio was significantly lower in the cilnidipine group ( p < 0.05 ) than in the amlodipine group. Amlodipine increased plasma angiotensin I and angiotensin II levels ( p < 0.05 ), whereas cilnidipine did not. Interestingly, the cilnidipine group had a higher ratio of angiotensin-(1–7) (Ang-(1–7)) to angiotensin II in plasma than the amlodipine group ( p < 0.05 ). Conclusions. The L-/N-type CCB cilnidipine, but not amlodipine, decreased urinary albumin excretion in hypertensive patients. Cilnidipine also increased the ratio of Ang-(1–7) to angiotensin II in plasma, which might be one factor underlying its beneficial effects.

Plasma Renin Activity, Plasma Angiotensin and Plasma and Urinary Electrolytes in Normal and Toxaemic Pregnancy, Including a Prospective Study

1973 ◽  
Vol 45 (1) ◽  
pp. 115-127 ◽  
Author(s):  
R. D. Gordon ◽  
E. M. Symonds ◽  
E. G. Wilmshurst ◽  
C. G. K. Pawsey
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Prospective Study ◽  
Plasma Renin ◽  
Late Pregnancy ◽  
Normal Pregnancy ◽  
Renin Activity ◽  
Creatinine Ratio ◽  
Plasma Angiotensin ◽  
A Prospective Study

1. In a prospective study involving fifty-six women, measurements of body weight, urinary creatinine, sodium and potassium and plasma sodium, potassium and renin activity were made in mid-pregnancy and at 36 weeks. The effect of sodium restriction and sodium loading on these measurements was assessed in mid-pregnancy. 2. Mean plasma renin activity was significantly higher throughout pregnancy than the normal non-pregnant mean level. It was lower at 36 weeks than in mid-pregnancy in those whose pregnancy was normal but not in those who developed toxaemia of pregnancy between 38 and 40 weeks. In mid-pregnancy in both groups sodium depletion was significantly elevated but sodium loading did not significantly depress plasma renin activity. 3. The urinary potassium/creatinine ratio in mid-pregnancy and urinary sodium/creatinine ratio at 36 weeks were lower in those who subsequently developed toxaemia, raising the possibility of a functional renal lesion which antedates the morphologically recognizable lesion of late pregnancy. 4. In a second study involving sixty-six different women plasma angiotensin II levels between 6 and 40 weeks of pregnancy were mostly above the normal range, and highest levels were observed between 21 and 30 weeks. The plasma angiotensin II levels in six women with established toxaemia of pregnancy were not significantly different from the levels in nine women with normal pregnancy of the same duration. 5. While the renal glomerular lesion is presumably the major determinant in the development of toxaemia, the heightened activity of the renin-angiotensin-aldosterone system which is appropriate to normal pregnancy is an aggravating factor in established toxaemia, and may predispose to its development in some patients by failing to decline in late pregnancy.

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