- Fetal Upturned Nose
- IgA Nephropathy in Pregnancy
- Umbilical vein varix
- Timing of Cranial Markers in Open NTD
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- Abnormal facial profile
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- Absent nasal bone (ANB)
- Choroid plexus cysts
- Chronic placental abruption
- Fetal Alcohol Syndrome
- Placenta-First Risk Stratification
- AVSD
- Blakes Pouch Cyst
- Confined Placental Mosaicism
- Echogenic Bowel
- Fetal Anemia
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- Fetal Mild Micromelia
- Hypochondroplasia – Mild Micromelia
- Hypoplastic Nasal Bone
- IgM IgG IgG Avidity
- Increased Nuchal Translucency
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- Partial agenesis of corpus callosum
- PGT A
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- Renal Pyelectasis or Extra Renal Pelvis
- Right And Double Aortic Arch
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- Y Microdeletion
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- Duodenal Atresia
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- Mutation Types in DMD
- Risk of rubella in nonimmune pregnant woman
- Salt-losing nephropathy
- Syndromic Cystic biliary atresia
- TGA DORV TOF CCTGA
- Unilateral echogenic kidney with polyhydramnios
- Unilateral renal agenesis, Ectopic, Cross fused kidney
Salt-losing nephropathy
Bartter syndrome
Most classic renal causes of severe polyhydramnios.
Mechanism
Defective tubular salt reabsorption leads to:
- massive fetal polyuria
- increased urine output
- severe polyhydramnios
Often:
- starts mid-trimester
- progresses rapidly
Ultrasound features
Typical pattern:
- polyhydramnios (often severe)
- normal or mildly enlarged kidneys
- kidneys may become echogenic
- bladder usually normal or large
Usually bilateral renal involvement, not unilateral.
Congenital nephrotic syndrome
Congenital nephrotic syndrome of the Finnish type; Diffuse mesangial sclerosis
These are glomerular disorders, not obstructive ones.
Mechanism of polyhydramnios
Occurs due to:
- fetal protein loss
- reduced plasma oncotic pressure
- increased urine production
Also:
- placentomegaly common
- maternal serum AFP may be elevated
Ultrasound features
- bilateral echogenic kidneys
- kidneys often enlarged
- polyhydramnios
- placentomegaly
bilateral involvement is typical.
Salt-losing nephropathy
- both kidneys echogenic
- progressive severe polyhydramnios
- kidneys not obstructed
- bladder normal
- placenta enlarged
Case
- unilateral PUJO
- progressive echogenicity
- CMD loss
- normal opposite kidney
- polyhydramnios
Most likely contralateral compensatory hyperfiltration
| Feature | PUJO progression | Bartter | Mesangial sclerosis |
|---|---|---|---|
| Laterality | Unilateral | Bilateral | Bilateral |
| Echogenicity | Unilateral | Bilateral | Bilateral |
| Polyhydramnios | Mild–moderate | Severe | Moderate–severe |
| Bladder | Normal | Large | Normal |
| Placenta | Normal | Normal | Enlarged |
Bartter
- very early severe polyhydramnios
- normal renal pelvis
- normal corticomedullary differentiation initially
- rapidly rising AFI
Congenital nephrotic syndrome
- placentomegaly
- bilateral large echogenic kidneys
- elevated maternal AFP
- early fetal edema
Unilateral PUJO → echogenic kidney + CMD loss + polyhydramnios - progressive unilateral obstructive nephropathy with preserved contralateral function
Salt-losing nephropathy or mesangial sclerosis: much less likely unless kidneys become bilaterally echogenic or polyhydramnios becomes severe and disproportionate.
Congenital mesoblastic nephroma
Most common fetal renal tumor.
- Tumor-induced polyuria
- Increased renal perfusion
- Occasionally hypercalcemia-related diuresis
Result: Often rapidly progressive polyhydramnios
Kidney appearance:
- Large unilateral renal mass
- Solid, homogeneous or slightly heterogeneous
- Often replaces normal kidney
- Kidney contour distorted
Doppler features: Marked vascularity
Mesoblastic nephroma
Typical sequence:
- Solid renal mass appears
- Kidney enlarges
- Mass grows
- Polyhydramnios develops
When mesoblastic nephroma SHOULD be suspected
- Kidney massively enlarged
- Solid renal mass seen
- Polyhydramnios rapidly worsening
- Doppler shows hypervascular lesion
- No clear obstructive pathway
Mesoblastic nephroma is unlikely when a kidney evolves from hydronephrosis to echogenic dysplastic appearance with CMD loss, because tumors present as solid enlarging masses rather than obstructive deterioration patterns.