NDT Advance Access originally published online on November 25, 2005
Nephrology Dialysis Transplantation 2006 21(2):522-525; doi:10.1093/ndt/gfi288
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Case Report
A 14-year-old girl with renal abnormalities after brief intrauterine exposure to enalapril during late gestation
1 Department of Nephrology, Institute of Internal Medicine, 2 Department of Pathology, Institute of Laboratory Medicine, 3 Department of Pediatrics, Institute for the Health of Women and Children and 4 Department of Clinical Physiology, The Cardiovascular Institute, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden
Correspondence and offprint requests to: Gregor Guron, MD, PhD, Department of Nephrology, Institute of Internal Medicine, The Sahlgrenska Academy at Göteborg University, Box 432, 405 30 Göteborg, Sweden. Email: gregor.guron@kidney.med.gu.se
Keywords: albuminuria; angiotensin-converting enzyme inhibitors; kidney development; renin–angiotensin system; urine-concentrating ability
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Introduction |
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In addition to its important role in the regulation of extracellular fluid homeostasis, an intact renin–angiotensin system (RAS) is essential for normal kidney development [1]. Several case reports have described fatal acute renal failure and renal tubular dysplasia in fetuses and newborns exposed to angiotensin-converting enzyme (ACE) inhibitors [2] or angiotensin II type-1 (AT1) receptor antagonists [3] during the second or third trimester. Notably, nephrogenesis is completed at about gestational week 36 in humans. Experimental studies have shown that interruption of the RAS during ongoing nephrogenesis, either pharmacologically or by gene knockout techniques, produces abnormalities in renal morphology and function that bear similarities to those described in case reports, and that normal kidney development is mainly mediated through the AT1 receptor [1,4,5]. Renal morphological abnormalities in these animals are characterized by papillary atrophy, wall thickening of pre-glomerular arterioles,
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