Long-term consequences in RAS blocker-induced fetopathy with multiorgan impairments.
Hiroshi Komatsu, Tomohiko Imai, Satoru Oya
✦ AI-curated · Sources linked
Case in brief
A girl with fetopathy after maternal exposure to a renin–angiotensin system blocker was followed for 10 years. She had severe short stature and persistent mild developmental delay; cranioplasty at 1 year revealed right frontal lobe hypertrophy. Episodes of marked polyuria caused hypernatremia, with evaluation indicating impaired collecting-duct water reabsorption attributed to aquaporin-2 dysfunction. At age 10, proteinuria prompted kidney biopsy, which showed chronic focal tubulointerstitial injury, hypertrophied remnant glomeruli with segmental sclerosis, and interlobular arterial thickening. Enalapril reduced the proteinuria.
What made this case unusual
The case documents persistent, multiorgan consequences over a decade, including collecting-duct water-handling impairment and chronic renal histologic changes after RAS blocker-induced fetopathy.
Diagnostic / clinical pearl
In RAS blocker-induced fetopathy, later polyuria and hypernatremia may reflect impaired collecting-duct water reabsorption, while proteinuria can accompany chronic renal injury; follow-up in this case identified both.
Why it matters
The reported developmental, growth, water-balance, and renal complications support the authors’ emphasis on long-term follow-up after RAS blocker-induced fetopathy.