As nephrogenesis continues until 36 weeks of gestation, very preterm babies (gestational age<32 weeks) are likely to show a nephron deficit at birth. In addition, preterm birth is known to be associated with impaired nephrogenesis and limited postnatal kidney growth until the age of 18–24 months. Birth weight appears to be a strong determinant of renal size, nephron number, glomerular volume, albuminuria and systolic blood pressure. These findings add weight to the hypothesis that IUGR carries a risk of renal function loss as a result of nephron deficit, loss of filtration surface area, hyperfiltration, glomerular hypertension, and glomerular damage. In the period immediately after birth, the short-term renal-related consequences of low birth weight are an increased risk of acute renal failure as well as transient imbalance of fluid and electrolyte homeostasis. When the number of nephrons is diminished, single-nephron GFR increases as the kidney works to compensate. In long term, this compensatory hypertrophy causes the glomeruli to function under increased intracapillary hydraulic pressure, which over time causes damage to the capillary walls. This abnormal process leads to progressive glomerulosclerosis, proteinuria, hypertension and chronic kidney disease. Over the past 20 years, evidence has been accumulated indicating that intrauterine growth restriction (IUGR) affects normal development of the kidneys and vascular system, thereby increasing the likelihood of hypertension and/or cardiovascular diseases. Impaired fetal kidney development leading to nephron deficit is considered an important pathway in the development of hypertension after IUGR birth. Apart from IUGR, premature birth may contribute to the development of disease at adult age.

Objective(s): To determine risk factors associated with IUGR in Bandar Abbas, Iran.Methods: This was a case-control study of live births. Cases were 60 newborns with less than 2500g weight at birth; controls were 60 newborns with birth weights above 2500g. Data were collected using a structured questionnaire and analyzed by the SPSS program.Results: Mother's employment (Odds Ratio=10.2, CI95%=1.2-87.3), hypertension (Odds Ratio=7.4, CI95%=1.5-36.9), lack of prenatal care (Odds Ratio=3.9, CI95%=1.2-13.7), and use of the hookah for smoking tobacco (Odds Ratio=3.5, CI95%=1.1-12.6) were found to be risk factors for intra-uterine growth retardation.Conclusion: To reduce IUGR we must identify high-risk women and educate them on the risks of IUGR and the ways to prevent this phenomenon.

Introduction: Intrauterine Growth Retardation (IUGR) is defined as approximate weight of embryo being less than the ten percentile. Some of the factors contributing to the IUGR are as follow: The mother history of chronic diseases, the mothers BMI, the trends of mother weight gain at the time of pregnancy, the mother’s age at the time of pregnancy, the mother’s job, various embryonic infections, placenta and uterine disorder. Materials and Methods: This cross-sectional, descriptive-analytical study was performed on pregnant women referring to the prenatal clinic of Baghiyatollah hospital at the years of 2009 and 2010 .Fifty hundred four  pregnant women, between the age of 18 and 35 years were examined as available, these following variable were surveyed: The mother’s age at the time of delivery, the mother’s BMI at early pregnancy, the mother’s weight gain during pregnancy, the mother history of chronic diseases, the age of pregnancy, the mother’s job and education, blood group and RH, gravid, the interval of deliveries, gender of newborn with IUGR. Data was analyzed by SPSS, chi-square and the logistic regression model.'Results: 60.3% had normal BMI, 29.2% had BMI higher than normal, and 10.5% had BMI lower than normal. 50% had normal weight gain, 31.7% had weight gain higher than normal, 13.1% had weight again lower than normal, 10.3% had a chronic disease, 15.1% were employed and 83.3%of women were educated.There was a significant relationship among the mother’s BMI at the beginning of pregnancy, the rate of mother’s weight again during pregnancy, the mother’s history of chronic disease, the mother’s job and the newborn’s gender with IUGR. Conclusion: Probability of IUGR is higher in woman whose weight gain was lower than normal rang, female newborn and housekeeper mothers. There is a direct link between IUGR and the history of chronic disease in mothers.

Background and Objectives: Perinatal morbidity and mortality are increased as much as 10 times in pregnancies complicated by IUGR, in comparison with normal pregnancy. For doing valid management decisions, accurate diagnosis is essential. Materials and Methods: In order to evaluate the accuracy of ultrasonography compares with clinical examination for detection of IUGR, we retrospectively reviewed medical records in pregnant mothers, who admitted to Taleghani and Al-Zahra Hospitals during 12 months and who had singletone deliveries. Results: We found that with one sonographic examination in second trimester, comparing with clinical examination, no significant differences were observed in diagnosis of IUGR, but with two sonographic examinations, one in second trimester and one in third trimester, there was a significant advantage upon clinical examination for detection of IUGR. Conclusion: This study provides strong evidences that at least two sonographic examinations, one in second trimester and one in third trimester, are essential for accurate diagnosis of IUGR, in order to reduce perinatal mortality and morbidity.    

Background and Aim: Given the significance of intrauterine growth restriction (IUGR) and the unclear mechanisms by which magnesium may prevent it, this study aimed to evaluate the growth response to magnesium supplementation in pregnant women at risk of IUGR in Kashan, Iran. Methods: This double-blind randomized clinical trial involved 70 women identified as being at risk for IUGR through uterine artery Doppler ultrasound. Women between 16 and 30 weeks of gestation were randomly assigned to two groups: one receiving a daily supplement of 250 mg of magnesium (n=35) and the other receiving a placebo (n=35) for a duration of 14 weeks. At the end of the study, biomarkers of oxidative stress (MDA, TAC, and GSH), lipid profile (total cholesterol, LDL-C, HDL-C, and triglycerides), insulin function parameters, inflammatory factors (hs-CRP and nitric oxide), and growth responses were assessed. Results: Daily magnesium supplementation for 14 weeks positively influenced the uterine artery resistance index in women at risk of IUGR. Following the intervention, magnesium supplementation resulted in a significant decrease in serum insulin levels and insulin resistance, alongside a notable increase in insulin sensitivity compared to the placebo group; however, there was no effect on fasting blood sugar levels. The serum levels of triglycerides, total cholesterol, LDL-C, and HDL-C in the magnesium group were comparable to those in the placebo group, showing no significant differences. Additionally, magnesium supplementation led to significant reductions in MDA, TAC, and hs-CRP compared to placebo, while GSH and nitric oxide levels remained similar between both groups with no significant differences. Conclusion: The findings of this study suggest that magnesium supplementation over a 14-week period positively impacts metabolic profiles and intrauterine growth in pregnant women at risk of IUGR.

Background: Gestational weight gain is an impressive factor in the fetal outcome. Intrauterine growth restriction (IUGR) is one of the most important problems during fetal period that may lead to many perinatal and long-term complications and growing neonatal morbidities and mortalities. The aim of the study was to ascertain the relationship between umbilical cord blood leptin concentration and fetal growth in neonates born with intrauterine growth restriction. Methods: Maternal serum and umbilical cord blood leptin concentration were measured by immune radiometric assay at term gestation. The study was conducted on 22 women with uncomplicated singleton pregnancies as control group (group A) and 22 women with fetal growth restriction in singleton pregnancies as case group (group B). All subjects had normal pregravid body mass index (BMI). Results: The results of the study showed that maternal serum leptin concentrations were significantly higher in group B comparing to group A (44ng/ml [28. 9-58. 2] vs. 24. 6ng/ml [18. 8-33. 3]; P<0. 001). However, umbilical cord blood leptin levels were significantly lower in group B comparing to group A (8. 6 ng/ml [range 4. 5-12. 7] vs. 14. 6 ng/ml [11. 7-16. 7]; P<0. 001). Moreover, umbilical cord blood leptin levels were directly correlated with maternal BMI and neonatal birth weight in both groups. Conclusion: In growth-restricted fetuses at term, umbilical cord blood leptin concentrations were significantly lower than normal fetuses, suggesting that fetal adipose tissue is a major source for leptin production. Maternal serum leptin concentrations were higher in the presence of a growth restricted fetuses. This increas may be due to early hypoxia or an intrinsic placental mechanism, by which small placenta produces more leptin as a compensatory mechanism. Human recombinant leptin may have some roles in the treatment of IUGR fetuses in future.

IUGR is a major causes and silent illness and death in the embryonic and infants population, which in it infants growth potential is less than natural state. IUGR phrase and small for gestation age often used interchangeably. Although, there is small difference between these two.IUGR/SGA as a result different etiology including maternal factors, placenta and fetus arise. That recently genetic factors added to it. IUGR may be caused by maternal smoking, infections agents and chromosomal or genetic abnormalities, maternal abnormalities, but in most cases secondary cause is placenta insufficiency. IUGR often causes complications in the third trimester of pregnancy which is associated with symptoms of preeclampsia.The pathophysiology of IUGR is associated with placenta insufficiency. It remains unclear, but the damage is usually caused due to failure of trophoblast invasion which causes intermittent blood flow the space between the intervillous that this also in turn causes local oxidative stress.