Intrauterine growth retardation leads to a permanent nephron deficit in the rat

Pediatr Nephrol. 1994 Apr;8(2):175-80. doi: 10.1007/BF00865473.

Abstract

Intrauterine growth retardation (IUGR) was induced in Sprague-Dawley rats by partial artery ligation of one uterine horn in the mother on day 17 of gestation or by feeding the mother a 5% protein diet from day 8 of gestation. The controls were pups of the contralateral uterine horn or pups born to mothers fed a normal (22%) protein diet. The number of nephrons present at birth and the final number of nephrons in 2-week-old rats were counted throughout the entire kidney. The number of nephrons present at birth and the final number of nephrons were significantly correlated with birth weight for growth-retarded rats of both groups and their corresponding controls (P < 0.02 for the poorest correlation). Clearance experiments and morphometric studies of 2-week-old rats born to mothers with uterine artery ligation indicated that, despite a large compensatory hypertrophy of the nephrons in those animals born with a nephron deficit of about 30%, the overall renal function was impaired. We conclude that IUGR is accompanied by a nephron deficit which may not be fully compensated for within the first weeks after birth.

MeSH terms

  • Animals
  • Disease Models, Animal
  • Female
  • Fetal Growth Retardation / complications*
  • Fetal Growth Retardation / embryology
  • Fetal Growth Retardation / physiopathology
  • Hypertrophy
  • Kidney Function Tests
  • Male
  • Nephrons / abnormalities*
  • Nephrons / pathology
  • Organ Size
  • Rats
  • Rats, Sprague-Dawley