Renal function during chronic anemia in the ovine fetus.

Our purpose was to determine how prolonged anemia alters fetal renal function and acid-base balance. In seven ovine fetuses made progressively anemic over 1 wk by serial isovolemic hemorrhage, hematocrit was reduced from 33.3 +/- 4.5 to 14.0 +/- 1.0%. Femoral arterial oxygen content 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 control fetuses (7.0 +/- 1.3 ml/dl and 160 +/- 34 ml.min-1.100 g kidney-1). Urine flow and sodium excretion were also greater in anemic fetuses (1.2 +/- 0.6 ml/min and 79 +/- 49.5 mumol/min) than in controls (0.5 +/- 0.2 ml/min and 16 +/- 9.8 mumol/min). This higher sodium excretion was apparently due to a lower fractional sodium reabsorption in 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 in anemic fetuses was associated with greater urinary lactate and inorganic phosphate excretions and larger amniotic fluid volumes than in controls. From these data we conclude that when fetal renal oxygen delivery is limited by a prolonged reduction in hematocrit, excretions of sodium and water, as well as other osmotically active solutes, increase, and this results in an increase in amniotic fluid volume.