Fluid-balance logic: from the second trimester onward fetal urine IS the amniotic fluid. So oligohydramnios = a urine-output problem until proven otherwise.
Apply this to each option:
Renal agenesis: no kidneys, no urine, severe early oligohydramnios with uterus smaller than dates. Perfect fit.
Fetal anemia: leads to high-output state and hydrops, which raise fluid (polyhydramnios), not reduce it, so it is the opposite direction and is out.
Bartter syndrome: a salt-wasting fetal tubulopathy classically associated with POLYhydramnios from fetal polyuria, so out.
Liddle syndrome: a sodium-retaining tubular channel disorder, not an oligohydramnios cause, so out.
Bottom line: the only option that abolishes fetal urine and gives marked early oligohydramnios is renal agenesis. Choose option a.