A broad range of epidemiological evidence supports the hypothesis that risk
of essential hypertension, coronary heart disease and non-insulin dependen
t diabetes is, in part, determined before birth. This phenomenon, termed pr
ogramming, is now the subject of intensive investigation in order to determ
ine possible underlying mechanisms. It is widely accepted that maternal nut
ritional status in pregnancy is a major programming influence upon the fetu
s. This review considers the hypothesis that nephron number in humans is de
termined by prenatal nutrition. An increasing number of human studies indic
ate that the developing kidney is particularly vulnerable to the adverse ef
fects of fetal growth retarding influences. In animals, growth retarding di
ets or other insults which have an impact upon the development of cardiovas
cular functions, also appear to impact upon nephron number. However, it is
possible that hy pertension and reduced renal reserve merely coincide and a
re not causally associated.