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1. This study was designed to examine the changes in kidney morphometry during gestation in fetuses that were either appropriate or small for gestational age and the relationship between umbilical vein plasma active renin and kidney morphometry. 2. Serial ultrasound measurements of various morphometric and renal indices were performed in a cohort of 87 singleton fetuses from 22 to 38 weeks gestation. Blood was collected from the umbilical vein at delivery and active renin was measured from the plasma based on angiotensinogen I generated during incubation with plasma and ox renin substrate. 3. Growth in the longitudinal plane of fetal kidneys was similar in the small- and appropriate-for-gestational age groups; however, growth in the anterio-posterior, transverse and circumference planes of the kidneys was significantly slower in the small-for-gestational-age group after 26 weeks gestation. Differences in growth rate in the two groups were most marked between 26 and 34 weeks and persisted until delivery when the anterior-posterior diameter was significantly larger (P < 0.00001) in the appropriate-for-gestational-age group (26.1 +/- 2.5 mm compared with 19.8 +/- 2.6 mm). The mean umbilical vein active plasma renin concentration at delivery was significantly higher (P < 0.05) in the small-for-gestation-age group (274.4 +/- 32.9 mu-units/ml plasma) than in the appropriate-for-gestational-age group (164.9 +/- 28.3 mu-units/ml plasma). In addition, there were statistically significant inverse correlations between renin concentration and birthweight (r = -0.55, P < 0.001) and between renin concentration and kidney anterior-posterior diameter (r = -0.67, P < 0.001). 4. Fetal renal growth was slower in small than in appropriate-for-gestational-age fetuses. The period of 26-34 weeks gestation was that during which maximum fetal renal growth occurred. Umbilical vein plasma renin levels were higher in small-for-gestational-age fetuses. The findings of slow fetal renal growth rate and associated high renin concentrations seen in small-for-gestational-age fetuses could be implicated in an irreversible reno-vascular pathology leading to adult hypertension. We suggest that 26 to 34 weeks could be the "critical period' during which the insult that leads to in-utero programming for the development of adult hypertension occurs.

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Objective To determine the structural characteristics of the rupture site of term fetal membranes (amniochorion and decidua) that rupture spontaneously after the onset of labour. Design Fourteen term fetal membranes were examined immediately after delivery at the light microscope level. Multiple samples were taken along the whole rupture site and along an axis between this site and placental edge. Morphometric analysis of the thickness of the constituent layers of the fetal membranes was performed. Setting Leicester Royal Infirmary Maternity Hospital. Results A restricted zone of extreme altered morphology, characterised by marked swelling and disruption of the connective tissue, thinning of the trophoblast layer and thinning or absence of decidua, was identified in the rupture site of all patients. Morphometric analysis of the thickness of membrane layers showed that these changes and the ratio between the thickness of the connective tissue layers and that of the trophoblast and decidua (termed fetal membrane morphometric index) were significant between the zone of extreme altered morphology and the rest of the membranes. Conclusions The morphological features of the zone of extreme altered morphology suggests that it represents an area of structural weakness of the membranes. Since this zone did not include the whole length of the rupture site, it is likely that it was present before membrane rupture and was generated during pregnancy. We hypothesise that the zone of extreme altered morphology represents the site of initial rupture after which the tear is transmitted through the membranes to produce the rupture site. It is possible that if these changes become more extreme, then prelabour membrane rupture may occur. Further characterisation of this zone may help to understand the mechanism of its genesis and its role in predisposing the fetal membranes to rupture.