Histologic study of the fetal offspring of maternal mice given 2,4,5‐trichlorophenoxy‐acetic acid (2,4,5‐T) suggested that the previously reported fetal “cystic kidneys” were due to a retardation in fetal renal development and downgrowth of the renal papilla into the pelvis. To determine a possible retardation in renal alkaline phosphatase or functional development, maternal mice received by gavage 60–120 mg/kg, 2,4,5‐T on days 6–14 of pregnancy. At necropsy on day 17, the fetal kidneys were excised and fixed 24 hr in cold 65% ethanol. Paraffin sections stained by Gomori's method revealed alkaline phosphatase mainly in tubules in the inner renal cortex. Fetal kidneys showing diminished or no alkaline phosphatase were designated subnormal. There was a statistically significant greater incidence of subnormal fetal kidneys in the 2,4,5‐T‐treated mice than in the untreated controls. In three experiments, some mice were also sacrificed on day 18, and the incidence of subnormal fetal kidneys was significantly lower than on day 17. This retardation in renal alkaline phosphatase development indicates a retardation in renal functional development and indirectly supports the view that 2,4,5‐T also retards the morphological development of the fetal kidney and is not a renal teratogen in mice. It also illustrates that selected histochemical studies may be helpful in a teratologic investigation.