Abstract
Since studies show that an unfavorable environment during intrauterine development predisposes individuals to several diseases in adulthood, our objective is to assess the relation between fetal growth restriction and chronic renal disease in adults. We searched four different electronic databases through November 2017: CENTRAL, EMBASE, LILACS and MEDLINE. We selected studies with longitudinal or transversal designs associating kidney function in adulthood with low birth weight. Two reviewers evaluated the inclusion criteria and the risk of bias and extracted data from the included papers. Thirteen studies were selected for the systematic review and meta-analysis. We observed increased risks of presenting end-stage renal disease (risk ratio 1.31, 95% confidence interval: 1.17, 1.47), a lower glomerular filtration rate (ml/min) (mean difference 7.14; 95% confidence interval: -12.12, -2.16), microalbuminuria (risk ratio 1.40; 95% confidence interval: 1.28, 1.52) and a small increase in the albumin/creatinine ratio (mean difference 0.46; 95% confidence interval: 0.03, 0.90) in the low birth weight patients, compared with control group. These findings suggest that low birth weight is associated with renal dysfunction in adults.
Highlights
The number of nephrons an individual has is determined before birth, and more than half of these develop in the last three months of pregnancy, up until 36 weeks [1,2]
Considering the 3 included studies that used microalbuminuria as an outcome, an increased risk of microalbuminuria was identified in the low birth weight group (RR 1.40; 95% CI: 1.28, 1.52) (Figure 5)
A small increase in the albumin-creatinine ratio was identified in the low birth weight group compared with the controls (MD 0.46; 95% CI: 0.03, 0.90) based on the 3 relevant included studies
Summary
The number of nephrons an individual has is determined before birth, and more than half of these develop in the last three months of pregnancy, up until 36 weeks [1,2]. Most studies have focused on fetal exposure to glucocorticoids in stressful situations as a plausible mechanism for reductions in the number of nephrons [8].
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