الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Human pregnancy is characterized by a dynamic change in
a variety of metabolic functions. The regulatory mechanisms
responsible for these changes in maternal protein, carbohydrate
and lipid metabolism have traditionally been ascribed
to the dramatic increase in circulating steroid and peptide
hormones. Pituitary growth hormone (HGH), a major regulatory
protein, has anabolic effects and stimulates protein
synthesis in many tissues including bone, muscle, connective
tissue and visceral organs. HGH also has profound effects on
carbohydrate and lipid metabolism (Herimee, 1979).
Increased concentrations of HGH and its variants were
recorded from midpregnancy until full-term (Kaplan and
Grumbach, 1964; Katz et al., 1969; Kletzky et al., 1985;
Frankenne et al., 1988), and placental GH (PGH) behaves as a
strong agonist to pituitary GH in binding to hepatic and
other HGH receptors (Frankenne et al., 1988}.
Furthermore, during normal pregnancy, glomerular filtration
rate (GFR) and renal plasma flow (RPF) were recorded to
increase by 30-50% above the pre-gravid values starting early
in pregnancy and reaching maxi.mum levels in the last trimester
(Dignam et al., 1958; Lindheimer and Katz, 1970;
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Introduction
Dunlop, 1981; Ronco et al., 1988). Also, kidney length was
reported to increase approximately one em during normal
pregnancy (Lindheimer and Katz, 1990; Kincaid-Smith, 1991).
On the other hand, more than forty years ago, it was
noticed that increased HGH levels in patients with acromegaly
were associated with an increase in renal size and function
(Barnett et al., 1943) and the administration of HGH to
normal human subjects led to a significant increase in GFR
and RPF (Corvilain and Abramow, 1962).
Recently, much argue arose regarding the effect of
increased GFR and RPF on the kidney function and morphology.
Some investigators attributed glomerular injury to the
increase in glomerular pressure (Brenner, 1983) and correlated
the increased glomerular size with mesangial sclerosis
(Doi et al., 1990). However, this effect was denied by other
workers (Baylis and Rennke, 1985).
So, it became the aim of the present work to study the
relationship between renal size, GFR and growth hormone (or
its variants with similar activity in maternal serum) during
different stages of pregnancy in comparison to non-pregnant
women, and to compare the results of multiparae with those of
primigravidae.
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