In utero exposure to non-steroidal anti-inflammatory agents (NSAIAs) can produce combinations of oligohydramnios, a bleeding diathesis, ileal perforation, premature closure of the ductus, and acute or chronic renal injury. NSAIAs induce renal dysgenesis in fetal monkeys and renal structural abnormalities in the developing human fetus. We report oligohydramnios and renal failure associated with in utero exposure to early, prolonged, high-dose indomethacin in four neonates, and to ibuprofen in one neonate. Four of the affected neonates were one of twins. In each set of twins, only one of the pair was affected. One set of twins was proven to be identical, whereas the other three sets seemed to be identical. It is possible that the histopathological findings of uncertain or incomplete tubular differentiation may be the result of a direct effect of NSAIAs on developing or "immature" tubules. Therefore, the advantages of NSAIAs as tocolytics need to be weighed against the complication of severe renal injury.

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