Obstructive nephropathy and the developing kidney: Too little or too much angiotensin?

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Although obstructive nephropathy remains a major cause of renal insufficiency in infants and children, current medical and surgical management is unsatisfactory. The response of the developing kidney to obstructed urine flow depends on the stage of renal development, and the severity of obstruction: obstruction early in nephrogenesis may lead to renal dysplasia, while obstruction later in nephrogenesis delays nephron maturation, and can result in reduced nephron number. In contrast to the adult, who can recover from even complete ureteral obstruction, the fetus and neonate are uniquely vulnerable; permanent sequelae may result despite the release of only several days of ureteral obstruction. Following the completion of nephrogenesis in normal development, structural and functional nephron maturation continues. While nephrogenesis is complete before birth in man and guinea pig, nephrogenesis continues 10 days after birth in the rat and mouse. Renal development at the time of birth in the rat and mouse is, therefore, analogous to that of the midtrimester human fetus, while renal maturation in the 14-day-old rat is analogous to that of the human infant. We have reported that in rats, three months following the relief of complete unilateral ureteral obstruction (UUO) from 14 to 19 days of age, renal growth is impaired, and nephron number is reduced1.