RENAL TUBULAR DAMAGE IN FETUSES WITH INTRAUTERINE GROWTH-RETARDATION

Fetal hypoxemia is one of the most frequent causes of intrauterine growth retardation (IUGR). In chronic fetal hypoxia, peripheral blood flow and blood flow to the kidneys is reduced to maintain heart, brain and adrenal perfusion, the 'brainsparing effect'. In kidneys the cells of the proximal tubules seem to be most sensitive to hypoxia caused by reduced blood flow. Damage to the cells of the proximal tubules can be easily diagnosed by urinary levels of N-acetyl-β-D-glucosaminidase (NAG), an enzyme present in high concentrations in these cells. The aim of the present study was to define the levels of NAG in the amniotic fluid, to diagnose damage to the cells of the proximal renal tubules in fetuses, and to correlate them with a detectable brain-sparing effect. The study was conducted on a total of 55 pregnancies: 9 pregnancies were complicated by IUGR, and the remaining 46 normal pregnancies formed the control group. Higher levels of NAG were detected in the amniotic fluid from the IUGR-complicated pregnancies (p < 0.025). In particular, fetuses with IUGR had high levels of NAG in the amniotic fluid in 8 of 9 cases (+ 2 SD compared with controls), while 1 had normal concentrations. In the 8 cases with high concentrations of NAG in the amniotic fluid, velocimetric Doppler study documented a brain-sparing effect, which was not present in the 1 fetus with normal NAG levels. In conclusion, high levels of NAG in the amniotic fluid may identify in uterus fetuses with renal damage. These individuals are in need of stricter peri- and postnatal care as, in the case of perinatal anoxia, this particular condition may be one of the causes concurrent in the onset of postnatal acute renal failure.