British Journal of Nutrition

Research Article

Effect of maternal iron restriction during pregnancy on renal morphology in the adult rat offspring

S. J. M. Lislea1, R. M. Lewisa2, C. J. Petrya2, S. E. Ozannea2, C. N. Halesa2 and A. J. Forheada1 c1

a1 Department of Physiology, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

a2 Department of Clinical Biochemistry, University of Cambridge, Adenbrooke's Hospital, Hills Road, Cambridge CB2 2QR, UK

Abstract

In rats, maternal anaemia during pregnancy causes hypertension in the adult offspring, although the mechanism is unknown. The present study investigated the renal morphology of adult rats born to mothers who were Fe-deficient during pregnancy. Rats were fed either a control (153 mg Fe/kg diet, n 7) or low-Fe (3 mg/kg diet, n 6) diet from 1 week before mating and throughout gestation. At delivery, the Fe-restricted (IR) mothers were anaemic; the IR pups were also anaemic and growth-retarded at 2 d of age. At 3 and 16 months, systolic blood pressure in the IR offspring (163 (sem 4) and 151 (sem 4) mmHg respectively, n 13) was greater than in control animals (145 (sem 3) and 119 (sem 4) mmHg respectively, n 15, P<0·05). At post mortem at 18 months, there was no difference in kidney weight between treatment groups, although relative kidney weight as a fraction of body weight in the IR offspring was greater than in control animals (P<0·05). Glomerular number was lower in the IR offspring (11·4 (sem 1·1) per 4mm2, n 13) compared with control rats (14·8 (sem 0·7), n 15, P<0·05). Maternal treatment had no effect on glomerular size, but overall, female rats had smaller and more numerous glomeruli per unit area than male rats. When all animals were considered, inverse relationships were observed between glomerular number and glomerular size (r−0·73, n 28, P<0·05), and glomerular number and systolic blood pressure at both 3 months (r−0·42, n 28, P<0·05) and 16 months of age (r−0·64, n 28, P<0·05). Therefore, in rats, maternal Fe restriction causes hypertension in the adult offspring that may be due, in part, to a deficit in nephron number.

(Received July 04 2002)

(Revised January 22 2003)

(Accepted January 22 2003)

Correspondence:

c1 *Corresponding author: Dr Alison J. Forhead, fax +44 1223 333840, email ajf1005@cam.ac.uk

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