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Literature DB >> 1771591

ACE inhibitor fetopathy and hypocalvaria: the kidney-skull connection.

Abstract

Two cases of angiotensin converting enzyme inhibitor fetopathy with renal tubular dysgenesis and severely underdeveloped calvarial bone are described. Six additional, unexposed cases of hypocalvaria are described, and possible links between calvarial development and fetal hypotension and/or chronic hypoxia are explored.

Entities: Disease Gene

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Year: 1991 PMID： 1771591 DOI： 10.1002/tera.1420440503

Source DB: PubMed Journal: Teratology ISSN： 0040-3709

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Cited

20 in total

Review 1. Drug-induced congenital defects: strategies to reduce the incidence.

Authors: M De Santis; B Carducci; A F Cavaliere; L De Santis; G Straface; A Caruso
Journal: Drug Saf Date: 2001 Impact factor: 5.606

2. Congenital renal tubular dysplasia and skull ossification defects similar to teratogenic effects of angiotensin converting enzyme (ACE) inhibitors.

Authors: D Kumar; G Moss; R Primhak; R Coombs
Journal: J Med Genet Date: 1997-07 Impact factor: 6.318

ACE inhibitor fetopathy and hypocalvaria: the kidney-skull connection.

Review 1. Drug-induced congenital defects: strategies to reduce the incidence.

2. Congenital renal tubular dysplasia and skull ossification defects similar to teratogenic effects of angiotensin converting enzyme (ACE) inhibitors.

3. Abnormal skull findings in neural tube defects.

4. Renovascular hypertension commencing during fetal life.

Review 5. Effects of maternally administered drugs on the fetal and neonatal kidney.

6. The extreme anterior domain is an essential craniofacial organizer acting through Kinin-Kallikrein signaling.

Review 7. An overview of the influence of ACE inhibitors on fetal-placental circulation and perinatal development.

8. Renal tubular dysgenesis and neonatal hemochromatosis without pulmonary hypoplasia.

9. Teratogenicity with angiotensin II receptor antagonists in pregnancy.

10. Angiotensin I-converting enzyme mutation (Trp1197Stop) causes a dramatic increase in blood ACE.