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

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).

Long‐term renal follow up of preterm neonates born before 35 weeks of gestation

“…SGA status of preterm infants has also been shown to affect the increase of apoptotic cells in the fetal kidney and to decrease renin and angiotensinogen. 17 Furthermore, the number and formation of nephrons are compromised, leading to lower fractional sodium excretion and GFR. 2,3,12,18 Specifically, Drougia et al found that SGA infants born before 34 weeks of gestation had significantly smaller kidneys at 24 months of age.…”

Epigenetic Mechanisms Responsible for the Transgenerational Inheritance of Intrauterine Growth Restriction Phenotypes

“…Therefore, few studies are carried out in humans, especially in growth restricted infants, to evaluate the association between IUGR and kidney disease. However, papers published by Wang et al in 2014 ( 9 ) and 2016 ( 41 ), respectively, were two of the rare studies that investigated the effect of human aberrant fetal growth environment on kidneys of fetuses. In both studies, fetuses and their kidney samples were collected from mothers who terminate their pregnancy due to preeclampsia ( 9 ), placental abruption, deformities of fetuses, and other intrauterine insults ( 41 ).…”

“…However, papers published by Wang et al in 2014 ( 9 ) and 2016 ( 41 ), respectively, were two of the rare studies that investigated the effect of human aberrant fetal growth environment on kidneys of fetuses. In both studies, fetuses and their kidney samples were collected from mothers who terminate their pregnancy due to preeclampsia ( 9 ), placental abruption, deformities of fetuses, and other intrauterine insults ( 41 ). Both papers reported negative effects that IUGR had on the fetuses, including significantly low birth weight (< 2 kg), approximately 0.4 times less nephron number, increased expression of pre-apoptosis proteins within kidney tissues ( 9 ), and reduced renal renin-angiotensinogen RNA levels by half the non-growth restricted fetuses ( 41 ).…”

Evaluation of PGP 9.5, NGFR, TGFβ1, FGFR1, MMP-2, AT2R2, SHH, and TUNEL in Primary Obstructive Megaureter Tissue

“…Some studies show increase of apoptotic epithelial, smooth muscle, and fibroblast cells in obstructive uropathy caused by ureteral obstruction or congenital ureteropelvic junction obstruction. [32][33][34][35] The aim of the study was to evaluate the appearance and distribution of different factors that participate in regulation, innervation, vascularization, and growth/ development of ureters and might take part of pathogenesis in development of POM.…”