title: Effects of ureteral obstruction on renal growth.
abstract: Renal insufficiency due to congenital obstructive nephropathy is a consequence of arrested or abnormal renal growth. A number of experimental studies have shown that the younger the age at the time of unilateral ureteral obstruction (UUO), the more severe the growth impairment of the ipsilateral kidney, and the greater the compensatory growth of the opposite kidney ("counterbalance"). Urinary obstruction in early fetal life results in renal dysplasia and a decrease in the number of functioning nephrons. The renin-angiotensin system is highly activated in early development, and UUO further increases this activity, resulting in vasoconstriction and glomerular contraction. Long-term UUO also causes progressive interstitial fibrosis, which presumably contributes to arrested growth of the kidney. This may result from excessive deposition of extracellular matrix stimulated by increased expression of transforming growth factor-beta 1. Neonatal UUO delays the expression of epidermal growth factor, and prolongs the expression of peritubular alpha smooth muscle actin, suggesting that renal maturation is delayed by UUO. Renal apoptosis is increased by UUO, which may contribute to the reduced DNA content of the neonatal obstructed kidney. Renal expression of clusterin, a glycoprotein associated with cell adhesion and protection from apoptosis, is increased by ipsilateral UUO, and also presumably modulates renal growth. Thus, renal growth and development are impaired by UUO through complex interactions between regulators of cell proliferation, cell destruction, and extracellular matrix.
authors.affiliation: Department of Pediatrics, University of Virginia, School of Medicine, Charlottesville 22908, USA.
authors.forename: R L
authors.initials: RL
authors.lastname: Chevalier
mesh_terms: D000375:Aging / Q000502:physiology; D000818:Animals; D006801:Humans; D007668:Kidney / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D014524:Urethral Obstruction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*