RENAL-FUNCTION DURING CHRONIC ANEMIA IN THE OVINE FETUS

Our purpose was to determine how prolonged anemia alters fetal renal f unction and acid-base balance. In seven ovine fetuses made progressive ly anemic over 1 wk by serial isovolemic hemorrhage, hematocrit was re duced from 33.3 +/- 4.5 to 14.0 +/- 1.0%. Femoral arterial oxygen cont ent was less and renal plasma flow was greater in anemic fetuses (1.5 +/- 0.1 ml/dl and 339 +/- 58 ml.min(-1).100 g kidney(-1)) than in 6 co ntrol fetuses (7.0 +/- 1.3 ml/dl and 160 +/- 34 ml.min(-1).100 g kidne y(-1)). Urine flow and sodium excretion were also greater in anemic fe tuses (1.2 +/- 0.6 ml/min and 79 +/- 49.5 mu mol/min) than in controls (0.5 +/- 0.2 ml/min and 16 +/- 9.8 mu mol/min). This higher sodium ex cretion was apparently due to a lower fractional sodium reabsorption i n anemic fetuses compared with controls (84.1 +/- 5.8 vs. 96.5 +/- 1.7 %), rather than to differences in either glomerular filtration rate or amount of filtered sodium. In addition, the higher sodium excretion i n anemic fetuses was associated with greater urinary lactate and inorg anic phosphate excretions and larger amniotic fluid volumes than in co ntrols. From these data we conclude that when fetal renal oxygen deliv ery is limited by a prolonged reduction in hematocrit, excretions of s odium and water, as well as other osmotically active solutes, increase , and this results in an increase in amniotic fluid volume.