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      Increased renal apoptosis and reduced renin–angiotensin system in fetal growth restriction

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          Abstract

          Objective:

          The purpose of the study was to characterize changes in apoptosis and the renin–angiotensin system (RAS) in fetal growth restriction (FGR).

          Materials and method:

          Fetuses were collected from patients who visited our hospital to either terminate or abort their pregnancy. Kidneys of fetuses which suffered with FGR, ( n=11) at gestational age of 33.4±0.5 weeks and those from non-FGR ( n=12) at gestational age of 34.3±0.9 weeks were collected. TUNEL, Bax and Bcl-2 staining were examined. The number of nephrons was also counted. Both protein and mRNA levels of renin and angiotensinogen were analyzed. Ultrasound was applied to measure fetus parameters including biparietal diameter, head circumference, circumference of abdomen, and femur length.

          Results:

          The number of nephrons was positively correlated with fetal weight at termination. Kidneys in the FGR group presented more apoptotic cells than those in the non-FGR group. Renin and angiotensinogen both decreased in the FGR group. Ultrasound revealed that biparietal diameter, abdomen circumference, femur length, and birth weight were all reduced in the FGR group compared with the non-FGR group. Kidney size was also restricted in the FGR group as indicated by ultrasound.

          Conclusion:

          Renal apoptosis might contribute to the reduction of nephrons, and ultrasound plays a vital role in early diagnosis of developmental origins of health and disease (DOHAD).

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          Most cited references65

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          Fetal origins of coronary heart disease.

          The fetal origins hypothesis states that fetal undernutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease. Animal studies have shown that undernutrition before birth programmes persisting changes in a range of metabolic, physiological, and structural parameters. Studies in humans have shown that men and women whose birth weights were at the lower end of the normal range, who were thin or short at birth, or who were small in relation to placental size have increased rates of coronary heart disease. We are beginning to understand something of the mechanisms underlying these associations. The programming of blood pressure, insulin responses to glucose, cholesterol metabolism, blood coagulation, and hormonal settings are all areas of active research.
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            Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales.

            Although the rise in ischaemic heart disease in England and Wales has been associated with increasing prosperity, mortality rates are highest in the least affluent areas. On division of the country into two hundred and twelve local authority areas a strong geographical relation was found between ischaemic heart disease mortality rates in 1968-78 and infant mortality in 1921-25. Of the twenty-four other common causes of death only bronchitis, stomach cancer, and rheumatic heart disease were similarly related to infant mortality. These diseases are associated with poor living conditions and mortality from them is declining. Ischaemic heart disease is strongly correlated with both neonatal and postneonatal mortality. It is suggested that poor nutrition in early life increases susceptibility to the effects of an affluent diet.
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              The uterine spiral arteries in human pregnancy: facts and controversies.

              Uterine spiral arteries play a vital role in supplying nutrients to the placenta and fetus, and for this purpose they are remodelled into highly dilated vessels by the action of invading trophoblast (physiological change). Knowledge of the mechanisms of these changes is relevant for a better understanding of pre-eclampsia and other pregnancy complications which show incomplete spiral artery remodelling. Controversies still abound concerning different steps in these physiological changes, and several of these disagreements are highlighted in this review, thereby suggesting directions for further research. First, a better definition of the degree of decidua- versus trophoblast-associated remodelling may help to devise a more adequate terminology. Other contestable issues are the vascular plugging and its relation with oxygen, trophoblast invasion from the outside or the inside of the vessels (intravasation versus extravasation), the impact of haemodynamics on endovascular migration, the replacement of arterial components by trophoblast, maternal tissue repair mechanisms and the role of uterine natural killer (NK) cells. Several of these features may be disturbed in complicated pregnancies, including the early decidua-associated vascular remodelling, vascular plugging and haemodynamics. The hyperinflammatory condition of pre-eclampsia may be responsible for vasculopathies such as acute atherosis, although the overall impact of such lesions on placental function is far from clear. Several features of the human placental bed are mirrored by processes in other species with haemochorial placentation, and studying such models may help to illuminate poorly understood aspects of human placentation.
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                Author and article information

                Journal
                J Renin Angiotensin Aldosterone Syst
                J Renin Angiotensin Aldosterone Syst
                JRA
                spjra
                Journal of the Renin-Angiotensin-Aldosterone System: JRAAS
                SAGE Publications (Sage UK: London, England )
                1470-3203
                1752-8976
                17 August 2016
                Jul-Sep 2016
                : 17
                : 3
                : 1470320316654810
                Affiliations
                [1-1470320316654810]Department of Obstetrics, Tianjin Central Hospital of Gynecology and Obstetrics, China
                Author notes
                [*]Xu Chen, 156 Nan Kai San Ma Lu, Tian Jin Central Hospital of Gynecology and Obstetrics, Nan Kai District, Tian Jin, P. R. China. Email: chenshutj@ 123456126.com
                Article
                10.1177_1470320316654810
                10.1177/1470320316654810
                5843940
                27534427
                2cdbda0d-803a-45bd-82d9-9b9b8f41bc4a
                © The Author(s) 2016

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License ( http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 9 November 2015
                : 5 April 2016
                Categories
                Original Article
                Custom metadata
                July-September 2016

                kidney disease,molecular,hormone,clinic analysis,fetal growth restriction,renin,angiotensinogen

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