Abstract
Fetal lower urinary tract obstruction [LUTO] represents a rare, heterogeneous group of uropathies involving mechanical or functional blockage at the bladder outlet of varying severity. While ultrasound is a fair screening tool for the antenatal detection of this condition, it cannot reliably determine the underlying etiology of LUTO presentations. Sonographic assessment of renal appearance and amniotic fluid volume, as well as urinary analyte analysis, are the most useful predictors of preserved renal function in fetal LUTO, although they, too, are limited in their ability to predict outcomes on an individual basis. Animal models suggest that obstructive uropathy likely causes irreparable damage to the renal and urinary collecting system injury early in pregnancy. When LUTO is associated with abnormal amniotic fluid volume, long-standing oligohydramnios may result in lethal pulmonary hypoplasia. Data evaluating the efficacy of vesicoamniotic shunt therapy for the treatment of fetal LUTO are inconclusive. While vesicoamniotic shunting may modify disease lethality by restoring fluid volume, renal and other genitourinary benefits are minimal if not altogether absent, arguably supporting the belief that bladder decompression is being performed after irreversible injury has already been sustained.
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