EMBRYONIC RENAL INJURY: A POSSIBLE FACTOR IN FETAL MALNUTRITION

Abstract

Chick embryo metabolism was monitored in a radlorespirometer where O2 consumption, CO2 production and 14CO2 from C-labeled proline, glutamate, aspartate and arginine was measured continuously during development. At nine days of development chemically dissimilar nephrotoxins (spermine, Na2 Cr2 O7, ethylene glycol monoethyl ether) were inoculated into the air sac which resulted in a temporary change in respiratory quotient from 0.71 to 0.85. At 18 days injured embryos consumed oxygen equal to that of a 14 day embryo and were 30-35% smaller in weight. Embryos with renal injury but matched with controls in terms of O2. utilization had a profound decrease in ability to metabolize the 14C-labeled substrates. Decreased ability to metabolize 14C-labeled proline was associated with decreased collagen formation. At 18 days there was pulmonary hypoplasia with sparce mesenchyme maturation but little residual evidence of renal injury that could be observed at ten days. It is suggested that renal injury during early fetal development may alter renal gluconeogenesis in addition to interfering with pathways essential for collagen formation, thereby contributing to fetal malnutrition and pulmonary hypoplasia. Supported by N.I.H. Grant HD08864.