Animal experiments have shown that after ureter obstruction hydronephrotic kidneys release increased amounts of prostaglandin E2(PGE2) and thromboxane A2(TxA2), suggesting that these prostanoids modify renal blood flow and excretory function in this model. To test the hypothesis that these mechanisms are also operative in congenital obstructive uropathy, we measured prostanoid excretion rates in 12 neonates and infants with congenital unilateral or bilateral hydronephrosis. Prostanoid determinations were performed by gas chromatography mass spectrometry. PGE2and thromboxane B2(TxB2) (non-enzymatic metabolite of TxA2) excretion exceeded the normal range in eight and 11 of 12 patients, respectively. Median PGE2excretion was 22, range 4-572 ng/h/1.73 m2 (normal 3-16). Median TxB2excretion was 22, range 3-188 ng/h/1.73 m2 (normal 3-7). No other renal prostanoids (prostaglandin F2a, 6-keto-prostaglandin F1alpha;) or systemic prostanoid metabolites (PGE-M, 2,3-dinorthromboxane B2, 11-dehydro-thromboxane B2, 2,3-dinor- 6-keto-prostaglandin FiJ were consistently elevated. A second group of 12 neonates with congenital obstructive uropathy was followed sequentially. PGE2and thromboxane B2excretion rates increased even further after surgical decompression and gradually normalized during follow-up. There was a significant relationship between elevated FeNa and enhanced PGE2and TxB2excretion. These data suggest that endogenous renal formation of PGE2 and TxA2is selectively stimulated in hydronephrotic kidneys in neonates and infants. PGE2and TxA2may be involved in modulating renal function in these infants.