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

C Merlet-Bénichou, T Gilbert, M Muffat-Joly… - Pediatric …, 1994 - Springer
C Merlet-Bénichou, T Gilbert, M Muffat-Joly, M Lelièvre-Pégorier, B Leroy
Pediatric nephrology, 1994Springer
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 …
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 overal 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.
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