Correct Answer: A. Renal agenesis
Renal agenesis (bilateral) is the classic cause of oligohydramnios in the second trimester. The fetus produces urine starting around 8–10 weeks of gestation, and by the second trimester, fetal urine accounts for approximately 80–90% of amniotic fluid volume. In bilateral renal agenesis (Potter syndrome), the kidneys fail to develop entirely, so no urine is produced. This results in severe oligohydramnios or anhydramnios, leading to a fundal height that lags behind the expected gestational age. The decreased amniotic fluid is the direct consequence of absent fetal urine production. Unilateral renal agenesis does not cause oligohydramnios because the contralateral kidney compensates. The combination of small-for-dates fundal height (24 weeks vs. expected 26 weeks) and ultrasonographic evidence of decreased amniotic fluid in the second trimester is pathognomonic for bilateral renal pathology, with renal agenesis being the most severe and most likely diagnosis in this clinical scenario.
Why the other options are wrong
B. Ureteral stricture — Ureteral stricture causes unilateral obstruction of urine flow. Even if bilateral, the obstruction occurs distal to the kidney, so urine is still produced and accumulates in the renal pelvis and ureter (hydronephrosis), not reducing amniotic fluid volume. Oligohydramnios occurs only when there is complete bilateral renal failure or absence of urine production. Stricture does not prevent urine formation—it merely obstructs its passage. C. Tracheoesophageal fistula — TEF is a respiratory/gastrointestinal anomaly that does not directly affect fetal urine production or amniotic fluid volume. While TEF may be associated with polyhydramnios (due to impaired fetal swallowing if the fistula is proximal), it does not cause oligohydramnios. The decreased amniotic fluid in this case is incompatible with TEF pathophysiology. TEF is detected by other ultrasound findings (absent gastric bubble, excessive drooling). D. Cardiac abnormalities — Cardiac defects cause oligohydramnios only if they result in severe fetal heart failure or reduced cardiac output, which impairs placental perfusion and fetal renal perfusion, thereby reducing urine output. However, most cardiac anomalies do not directly abolish urine production. The primary mechanism of oligohydramnios in this case is absent urine production, not secondary renal hypoperfusion. Cardiac anomalies are more commonly associated with polyhydramnios (e.g., in high-output states or when associated with other anomalies).
High-Yield Facts
- Fetal urine accounts for 80–90% of amniotic fluid by the second and third trimesters; bilateral renal failure → oligohydramnios.
- Bilateral renal agenesis (Potter syndrome) presents with severe oligohydramnios/anhydramnios, small-for-dates fundal height, and characteristic facial features (low-set ears, micrognathia, hypertelorism).
- Unilateral renal agenesis does NOT cause oligohydramnios because the contralateral kidney compensates with increased urine production.
- Oligohydramnios in second trimester is a red flag for bilateral renal pathology; differential includes bilateral agenesis, bilateral dysplasia, bilateral obstruction (rare).
- Fundal height lag (24 weeks at 26 weeks gestation) combined with decreased amniotic fluid on ultrasound is the key clinical clue pointing to renal pathology.
Mnemonics
URINE = 80% AFV Urine = 80% of Amniotic Fluid Volume in 2nd/3rd trimester. No kidneys → No urine → No fluid. Use this when you see oligohydramnios + small-for-dates in mid-pregnancy. Potter = Bilateral Renal Agenesis Potter = Perfect storm of bilateral renal failure. Remember: Potter's face (low ears, micrognathia) + Potter's oligohydramnios (severe) + Potter's prognosis (incompatible with life if bilateral). Unilateral? No problem—other kidney works.
NBE Trap
NBE pairs oligohydramnios with various fetal anomalies to test whether students understand the mechanism of amniotic fluid production. The trap is selecting ureteral stricture or cardiac disease because they are "renal-related" or "can affect fluid balance," when the discriminating fact is that only bilateral renal absence or failure prevents urine production entirely. Stricture and cardiac disease do not abolish urine formation.
Clinical Pearl
In Indian obstetric practice, when a second-trimester scan shows oligohydramnios with small-for-dates fundal height and no other obvious anomaly, bilateral renal agenesis (Potter syndrome) is the diagnosis to rule out first. Detailed fetal renal ultrasound (absence of both kidneys, absent bladder) and maternal serum alpha-fetoprotein elevation support the diagnosis. Counseling for poor prognosis and neonatal intensive care readiness is essential.
_Reference: DC Dutta's Textbook of Obstetrics (7th ed.), Ch. 9 (Fetal Abnormalities); Harrison's Principles of Internal Medicine, Ch. 297 (Genetic Disorders of the Kidney)_