Gleason C A
Semin Perinatol. 1987 Jan;11(1):12-21.
Prostaglandins PGE2, PGD2, PGI2, and PGF2 alpha, as well as thromboxanes and leukotrienes, are synthesized by the fetal and neonatal kidney. The major prostaglandin, PGE2, PGD2, and PGI2, increase RBF, free water clearance, urine flow, and natriuresis. Alterations in the synthetic and catabolic activity of renal prostaglandins with advancing gestational and postnatal age occur along with concomitant alterations in RBF, GFR, and water and electrolyte excretion, suggesting that the prostaglandins play an important role in renal functional development. Indomethacin treatment may affect both fetal and neonatal renal function. Long-term maternal indomethacin treatment may decrease fetal urine output enough to alter amniotic fluid volume. Neonatal indomethacin therapy may cause transient dose-related renal dysfunction characterized by a decrease in urine output, but this renal dysfunction also depends in part on dosage, timing of therapy, and the cardiovascular and renal status of the infant prior to treatment. New areas of research interest include urinary prostaglandins as a marker for development of essential hypertension, and the possible interaction between antenatal steroids and renal function in the newborn.
前列腺素PGE2、PGD2、PGI2和PGF2α，以及血栓素和白三烯，由胎儿和新生儿的肾脏合成。主要的前列腺素PGE2、PGD2和PGI2可增加肾血流量、自由水清除率、尿量和尿钠排泄。随着胎龄和出生后年龄的增长，肾脏前列腺素合成和分解代谢活性的改变与肾血流量、肾小球滤过率以及水和电解质排泄的相应改变同时发生，这表明前列腺素在肾脏功能发育中起重要作用。吲哚美辛治疗可能会影响胎儿和新生儿的肾功能。母亲长期使用吲哚美辛治疗可能会使胎儿尿量减少到足以改变羊水量。新生儿使用吲哚美辛治疗可能会导致与剂量相关的短暂肾功能障碍，其特征为尿量减少，但这种肾功能障碍也部分取决于剂量、治疗时间以及治疗前婴儿的心血管和肾脏状况。新的研究热点包括将尿前列腺素作为原发性高血压发病的标志物，以及产前类固醇与新生儿肾功能之间可能存在的相互作用。
