# Neonatal Renal Failure Following Intrauterine Exposure to an Angiotensin-Converting Enzyme Inhibitor

**Authors:** Inês Rodrigues, Carolina Quintela, Joana Jardim, Helena Pinto, Susana Pissarra, Henrique Soares, Paulo Soares

PMC · DOI: 10.7759/cureus.53833 · Cureus · 2024-02-08

## TL;DR

A baby developed kidney failure after being exposed to a blood pressure drug in the womb, highlighting risks of such medications during pregnancy.

## Contribution

This case report adds to evidence that third-trimester exposure to ACE inhibitors can cause neonatal renal failure.

## Key findings

- A 39-year-old pregnant woman taking enalapril delivered a baby with anuria and acute renal failure.
- The infant's kidney function normalized after 48 hours of supportive care.
- Low angiotensin-converting enzyme levels were observed in the infant.

## Abstract

The renin-angiotensin-aldosterone system (RAAS) plays a crucial role in the normal development of the fetal kidney. Late pregnancy blockage of the RAAS, through in-utero exposure to angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers, is associated with poor fetal outcomes, including oligohydramnios, renal tubular dysplasia, postnatal anuric renal failure, and hypotension. The present case describes a 39-year-old primigravida that was referred to the emergency department, at 37 weeks, for the evaluation of intrauterine growth restriction and suspected coarctation of the aorta (CoA). She was medicated with enalapril since the 35th week of gestation. She delivered a male infant, weighing 2,110 g, with no apparent malformations. CoA was excluded. During his first day of life, the patient developed anuria, acute renal failure, and hypotension, requiring ionotropic support. Renal ultrasound appeared normal. Diuresis was reinitiated at 48 hours of life after continued supportive measures. Kidney function tests progressively normalized. Additional investigations revealed a low concentration of angiotensin-converting enzyme. The patient is currently 12 months old and has had a favorable evolution. This case highlights the fact that even brief exposure to enalapril in the third trimester may cause RAAS blocker fetopathy. As long-term sequelae of ACEI-exposed infants are poorly described, close follow-up of renal complications is essential. Physicians should be aware of the deleterious effects of RAAS blockers in pregnancy.

## Linked entities

- **Chemicals:** enalapril (PubChem CID 5388962)
- **Diseases:** renal failure (MONDO:0001106), hypotension (MONDO:0005468), intrauterine growth restriction (MONDO:0005030), coarctation of the aorta (MONDO:0007345)

## Full-text entities

- **Genes:** REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}
- **Diseases:** renal complications (MESH:D007674), hypotension (MESH:D007022), acute renal failure (MESH:D058186), intrauterine growth restriction (MESH:D005317), renal tubular dysplasia (MESH:D000141), fetopathy (MESH:C576203), malformations (MESH:C564254), anuria (MESH:D001002), oligohydramnios (MESH:D016104), Neonatal Renal Failure (MESH:D051437), CoA (MESH:D001017)
- **Chemicals:** enalapril (MESH:D004656), RAAS blockers (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

7 references — full list in the complete paper: https://tomesphere.com/paper/PMC10924429/full.md

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Source: https://tomesphere.com/paper/PMC10924429