TY - JOUR
T1 - Renin Angiotensin System Blocker Fetopathy
T2 - A Midwest Pediatric Nephrology Consortium Report
AU - Nadeem, Shahid
AU - Hashmat, Shireen
AU - Defreitas, Marissa J.
AU - Westreich, Katherine D.
AU - Shatat, Ibrahim F.
AU - Selewski, David T.
AU - Onder, Ali M.
AU - Chiang, Myra
AU - Weaver, Donald J.
AU - Steinke, Julia
AU - Barcia, John
AU - Hernandez, Joel
AU - Hidalgo, Guillermo
AU - Ingraham, Susan E.
AU - Abitbol, Carolyn L.
AU - Pan, Cynthia
AU - Greenbaum, Larry A.
N1 - Publisher Copyright:
© 2015 Elsevier Inc.
PY - 2015/10/1
Y1 - 2015/10/1
N2 - Objectives Fetuses continue to be exposed to renin angiotensin system (RAS) blockers despite their known teratogenicity and a black box warning. We hypothesized that fetopathy from in utero exposure to RAS blockers has a broader spectrum of clinical manifestations than described previously and that there are a variety of clinical scenarios leading to such exposures. Study design This was a retrospective study performed through the Midwest Pediatric Nephrology Consortium. Cases of RAS blocker fetopathy were identified, with determination of renal and extrarenal manifestations, timing of exposure, and the explanation for the fetal exposure. Results Twenty-four cases were identified. RAS blocker exposure after the first trimester was associated with more severe renal manifestations. Chronic dialysis or kidney transplantation was required in 8 of 17 (47%) patients with RAS blocker exposure after the first trimester and 0 of 7 patients with exposure restricted to the first trimester (P = .05). Extrarenal manifestations, some not previously noted in the literature, included central nervous system anomalies (cystic encephalomalacia, cortical blindness, sensorineural hearing loss, arachnoid cysts) and pulmonary complications (pneumothorax, pneumomediastinum). RAS blocker exposure usually was secondary to absent or poor prenatal care or undiagnosed pregnancy. Conclusion RAS blocker fetopathy continues to be a cause of considerable morbidity, with more severe renal manifestations associated with exposure after the first trimester. A variety of significant extrarenal manifestations occur in these patients. Clinicians should emphasize the risk of fetopathy when prescribing RAS blockers to women of childbearing age.
AB - Objectives Fetuses continue to be exposed to renin angiotensin system (RAS) blockers despite their known teratogenicity and a black box warning. We hypothesized that fetopathy from in utero exposure to RAS blockers has a broader spectrum of clinical manifestations than described previously and that there are a variety of clinical scenarios leading to such exposures. Study design This was a retrospective study performed through the Midwest Pediatric Nephrology Consortium. Cases of RAS blocker fetopathy were identified, with determination of renal and extrarenal manifestations, timing of exposure, and the explanation for the fetal exposure. Results Twenty-four cases were identified. RAS blocker exposure after the first trimester was associated with more severe renal manifestations. Chronic dialysis or kidney transplantation was required in 8 of 17 (47%) patients with RAS blocker exposure after the first trimester and 0 of 7 patients with exposure restricted to the first trimester (P = .05). Extrarenal manifestations, some not previously noted in the literature, included central nervous system anomalies (cystic encephalomalacia, cortical blindness, sensorineural hearing loss, arachnoid cysts) and pulmonary complications (pneumothorax, pneumomediastinum). RAS blocker exposure usually was secondary to absent or poor prenatal care or undiagnosed pregnancy. Conclusion RAS blocker fetopathy continues to be a cause of considerable morbidity, with more severe renal manifestations associated with exposure after the first trimester. A variety of significant extrarenal manifestations occur in these patients. Clinicians should emphasize the risk of fetopathy when prescribing RAS blockers to women of childbearing age.
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U2 - 10.1016/j.jpeds.2015.05.045
DO - 10.1016/j.jpeds.2015.05.045
M3 - Article
C2 - 26130112
AN - SCOPUS:84952881850
SN - 0022-3476
VL - 167
SP - 881
EP - 885
JO - Journal of Pediatrics
JF - Journal of Pediatrics
IS - 4
ER -