Bartter syndrome, which presents clinically with polyuria, urinary potassium 
loss, hypokalemia, hypercalciuria, and alkalosis, is an autosomal recessive 
disorder with mutations in genes encoding the Na-K-2Cl cotransporter, the 
chloride channel CLC-NKB, and the potassium channel ROMK. Prenatal diagnosis of 
Bartter syndrome is now possible; however, there are no reports of the placental 
pathology associated with fetal Bartter syndrome. We present the placental 
pathologic findings in two siblings with fetal Bartter syndrome. Both 
pregnancies were complicated by polyhydramnios and preterm delivery. The first 
pregnancy delivered at 30 weeks, and Bartter syndrome was diagnosed in the 
perinatal period. The subsequent pregnancy required periodic therapeutic 
amniocentesis secondary to massive polyhydramnios and delivered at 32 weeks 
gestation. The suspicion of fetal Bartter syndrome was very high in this second 
pregnancy, and the infant was confirmed to have Bartter syndrome subsequently. 
Both placentas were large for gestational age, weighing greater than the 95th 
percentile. Microscopic examination showed extensive subtrophoblastic basement 
membrane mineralization (special stains positive for iron and calcium) in the 
chorionic villi. This striking finding was present in both placentas. 
Subtrophoblastic mineralization has been described in the literature in 
placentas of fetuses with abnormalities including anencephaly, trisomy 21, and 
other congenital abnormalities; however, it has also been described in normal 
pregnancies. Mechanisms of calcification in the placenta are not well 
understood, but these striking cases suggest that defects in fetal renal 
excretion of ions can lead to dystrophic calcification within the placenta, 
particularly in a subtrophoblastic pattern.