Embryology · Teratology and prenatal diagnosis
ACE inhibitors and ARBs: fetal kidney damage !
- Teratogen
Some blood pressure medicines damage the fetal kidneys in the second half of pregnancy and leave too little amniotic fluid.
Updated 2026-11-01
See it in 3D: Kidneys · Parietal bones
What it is
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) cause a fetopathy rather than a classic embryopathy: damage appears mostly with exposure in the second and third trimesters. The fetal kidney needs angiotensin II to maintain filtration and build its tubules; without it fetal urine falls and oligohydramnios follows, with consequences for the lungs, limbs and skull.
Key facts
- Oligohydramnios can reverse if exposure ends in time.
- Direct renin inhibitors share this mechanism.
- Renal tubular dysgenesis also exists as a genetic disease of renin–angiotensin system genes.
- Patent ductus arteriosus and fetal or neonatal death have been described.
- An example of 'no stage is safe': the damage happens outside the embryonic period.
Critical period and mechanism
- Critical period: second and third trimesters, when the fetal kidney makes most of the amniotic fluid.
- Angiotensin II constricts the efferent arteriole and maintains fetal glomerular filtration pressure.
- Blocking it lowers filtration, disturbs tubular development and reduces fetal urine.
- Lack of amniotic fluid compresses the fetus and prevents normal lung growth; poor perfusion affects the skull.
Prevention
- Planning blood pressure control with the treating professional before and during pregnancy.
- Medicines in pregnancy are decided with the treating professional; they are not stopped on one's own.
- Ultrasound monitoring of amniotic fluid after an exposure.
What it does to the embryo and fetus
- Oligohydramnios or anhydramnios on ultrasound; echogenic kidneys.
- At birth: anuria, renal failure, hypotension.
- Pulmonary hypoplasia with respiratory distress, limb contractures.
- Poorly ossified skull bones, growth restriction, fetal or neonatal death.
Test yourself
Think of the answer, then tap the question to see it.
In which trimesters are ACE inhibitors and ARBs most harmful to the fetus?
The second and third trimesters.
Why do ACE inhibitors cause oligohydramnios?
Without angiotensin II fetal glomerular filtration falls and tubular development is disturbed, so the fetus makes little urine.
What are the consequences of that oligohydramnios?
Pulmonary hypoplasia, joint contractures and facial deformation, as in the Potter sequence.
See it in 3D
The structures of Durgical's 3D anatomy where it is found.
Related
- Renal agenesis and the Potter sequence
- Amniotic fluid: polyhydramnios and oligohydramnios
- Pulmonary hypoplasia
- Kidney: pronephros, mesonephros, metanephros and ascent
- Patent ductus arteriosus
- Skull: neurocranium, viscerocranium, sutures and fontanelles
- Malformation, disruption, deformation, sequence, syndrome, association
Related conditions
In Pharmacology
Educational content on embryonic development; not a guide to prenatal diagnosis or to medicines in pregnancy and no substitute for a health professional's advice. No doses are given.
Sources: Angiotensin‐II receptor 1 antagonist fetopathy (PubMed Central (NCBI), 2012); Langman's Medical Embryology, 13th ed., ch. 9: Birth Defects and Prenatal Diagnosis (Wolters Kluwer, 2015).
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Representative model, for educational purposes only.