Prenatal Imaging and Intervention

Overview and Imaging.

Fetal kidneys can be identified at 13 weeks of gestation. Normal renal sizes through gestation (mean kidney length in millimeters is slightly longer than weeks of gestation) are shown in Table 112.1 . Corticomedullary differentiation is apparent by 20 weeks of gestation ( Fig. 112.1 ). Renal calyces and ureters typically are not seen on ultrasound unless they are pathologically dilated, and the renal pelvis is only readily visualized once the anterior-posterior diameter exceeds 2 mm. The fetal bladder can be visualized at 10 weeks of gestation. The bladder wall should not measure more than 3 mm. Bladder wall thickening may be a sign of outlet obstruction.

Amniotic fluid volume can be a reflection of renal health. Oligohydramnios (defined by an amniotic fluid index less than 8 cm) may be seen in the setting of placental insufficiency, intrauterine growth retardation, chromosomal abnormality, premature rupture of membranes, post-dates gestation, or urologic pathology ( Box 112.1 ).

Overview.

Fetal renal echogenicity may be abnormally increased as a normal variant but more often reflects an underlying abnormality. The fetal kidney is considered echogenic if it is brighter than the fetal liver. Echogenic kidneys are observed in approximately 1 to 2 per 1000 fetal ultrasounds, and approximately 10% of cases of renal malformations include echogenic kidneys. Etiologic considerations for the echogenic kidney are summarized in Box 112.2 . If echogenic kidneys are identified and the amniotic fluid volume is normal, the findings suggest nonlethal renal disease. Echogenic kidneys with oligohydramnios are highly concerning for a poor outcome.

Overview.

Congenital cystic renal diseases occur in about 2 to 4 in 1000 live births and include autosomal dominant and autosomal recessive polycystic kidney disease ( Fig. 112.2 and Video 112.1 ), multicystic dysplastic kidney ( Fig. 112.3 ), cystic glomerulopathies, and other cystic renal dysplasias. The complex pathogenesis of these disorders involves an abnormal orchestration of transcription and growth factor expression ( Table 112.2 ), as well as ciliopathies affecting the renal tubule primary cilium ( Table 112.3 ). Structural and functional abnormalities in primary cilia contribute to various cystic phenotypes that involve the kidney and liver.