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Levels of sodium and calcium ions and beta-2-microglobulin in fetal urine may be a useful indicator of prenatal kidney function in suspected cases of obstructive uropathy. Obstructive uropathy of the lower urinary tract can arise from urethral valves that block urination. In determining which cases of obstruction may benefit from prenatal surgery, it is important to assess kidney function. Of 25 fetuses with lower urinary tract obstructions, 23 were diagnosed with urethral valve obstruction. Of the 16 that were terminated or died before or after birth, all had urethral valve obstructions. In the urine samples, levels of sodium and calcium ions were significantly higher in those who died as newborns than those who survived. The two infants without urethral valve obstruction had normal concentrations of sodium and calcium ions in their urine. Furthermore, of the fetuses with beta-2-microglobulin levels over 13 milligrams per liter, all but one died.

OBJECTIVE: The etiology of oligohydramnios-related pulmonary hypoplasia is not understood but is known to involve chronic lung liquid loss. We tested the hypothesis that low amniotic pressure in oligohydramnios disturbs the normal tracheal-amniotic pressure gradient to increase lung liquid loss and impair lung development. STUDY DESIGN: Chronic pharyngeal catheterization with drainage to the exterior was used in 15 fetal sheep to mimic reduced amniotic pressure at the upper airway in the presence of normal amniotic fluid volume. RESULTS: Pharyngeal pressures relative to amniotic pressures were negative in all drained fetuses (mean [+ or -] SE -3.0 [+ or -] 0.6 mm Hg), in contrast to positive pressures in controls (0.7 [+ or -] 0.1 mm Hg). There was no significant difference in lung weight or deoxyribonucleic acid relative to body weight, or in lung morphometry, between 10 fetuses drained for 10 to 21 days and their control cotwins. CONCLUSION: Mimicking low amniotic pressure in the upper airway by chronic fetal pharyngeal drainage does not impair lung development in fetal sheep. (Am J Obstet Gynecol 1992;166:991-6.)

Pulmonary hypoplasia, the underdevelopment of fetal lung tissue, can cause fetal death. Within the uterus the fetus is surrounded by amniotic fluid. Although there are many factors predisposing the fetus to pulmonary hypoplasia, one theory suggests that an inadequate amount of amniotic fluid, oligohydramnios, is responsible. Pulmonary hypoplasia occurs because the uterine wall compresses the fetal chest which in turn compresses the lung tissue, inhibiting growth. This theory does not explain why tissue compression does not affect the development of other organs. Another theory explains that the pressure of the amniotic fluid, amniotic pressure, is decreased when the fluid volume is reduced; decreased amniotic pressure causes too much fluid to be lost from the fetal lungs. Pressure inside the small structures of the lungs must be greater than the amniotic pressure to promote growth and function. If that balance is upset, as in oligohydramnios, too much fluid escapes from the fetal lungs. To prevent this from happening the amniotic fluid volume must be increased by adding more fluid artificially. Amniotic fluid replacement was attempted in one pregnancy with oligohydramnios. Although the fetus died from other complications, the fetal lungs had no evidence of fetal lung hypoplasia.

Adequate fetal growth requires the transfer of nutrients and oxygen from the mother to the fetus. When this is compromised, abnormal fetal growth can result. Glucose, a simple sugar, is transferred from the mother to the fetus through the placenta. Various investigators have reported contrasting results regarding the amounts of glucose concentrations found throughout pregnancy. Glucose concentrations during pregnancy were measured in 25 normal pregnancies, 13 pregnancies complicated by blood incompatibilities, and 16 showing abnormal fetal growth patterns. Although the glucose measurements in the mother were similar and adequate in all the groups, the concentrations in the fetuses differed. The growth-retarded fetuses had lower glucose concentrations and less circulating oxygen than those of normal pregnancies. The group having blood incompatibility had higher glucose concentrations. It is suggested that there is a relationship between the concentrations of glucose, oxygen-carrying capacity of the blood and growth retardation. How these altered concentrations affect fetal growth requires further investigation.