Objective: To investigate the effect of Type II (asymmetrical) intrauterine growth retardation (IUGR) on renal development.
Design: A prospective descriptive study.
Setting: Department of Fetal and Infant Pathology, Liverpool Children's Hospital.
Subjects: Six (severely) affected IUGR stillbirths of known gestational age with a control group of stillbirths with birthweight greater than 10th centile, and eight liveborn IUGR infants who died within a year of birth with a control group of appropriately grown infants who died within a year of birth (postnatal groups).
Techniques: The kidneys from all the groups studied were analysed using unbiased, reproducible and objective design-based stereological techniques.
Main outcome measures: Total renal nephron (glomerular) numbers and average volumes of total nephron and cortical and medullary nephron segments.
Results: Nephron number estimates lay below the control group's 5% prediction limit in five out of the six growth-retarded stillbirths, and were significantly (P less than 0.005, IUGR at 65% of the control mean) reduced in the postnatal group. Estimates of nephron (segment) volume did not differ between control and IUGR groups.
Conclusions: Type II intrauterine growth retardation may exert a profound effect on renal development. The reduced nephron number at birth, together with the lack of any early postnatal compensation in either nephron number or nephron size, emphasizes the need for vigorous antenatal surveillance for IUGR and consideration of elective preterm delivery of affected fetuses. A systematic review of other organs, which develop in a similarly rapid fashion during the late intrauterine period, is indicated by this work. With one exception, all birthweights in the growth-retarded groups were below the third centile, thus the precise quantitative relation between progressive IUGR and renal function requires further assessment.