@article{d133985869e543e48fc9a3e3333760a4,
title = "Fetal—Not Maternal—APOL1 Genotype Associated with Risk for Preeclampsia in Those with African Ancestry",
abstract = "Black Americans are at increased risk for preeclampsia. Genetic variants in apolipoprotein L1 (APOL1) account for much of the increased risk for kidney disease in blacks. APOL1 is expressed in human placenta and transgenic mice expressing APOL1 develop preeclampsia. We evaluated the role of APOL1 variants in human preeclampsia. We determined maternal and fetal APOL1 genotypes in black women with preeclampsia in two populations. At Einstein Montefiore Center (EMC) Affiliated Hospitals, we studied 121 pregnancies in black women with preeclampsia. At University of Tennessee Health Science Center (UTHSC), we studied 93 pregnancies in black women with preeclampsia and 793 pregnancies without preeclampsia. We measured serum markers of preeclampsia soluble fms-like tyrosine kinase 1 (sFlt-1), placental growth factor (PlGF), and soluble endoglin (sEng). Fetal APOL1 high-risk (HR) genotype was associated with preeclampsia, with odds ratios at EMC and UTHSC of 1.84 (95% CI 1.11, 2.93) and 1.92 (95% CI 1.05, 3.49), respectively. Maternal APOL1 HR genotype was not associated with preeclampsia. Mothers with the fetal APOL1 HR genotype had more cerebral or visual disturbances (63% versus 37%, p = 0.04). In addition, fetal APOL1 HR genotype was associated with a higher sFLT-1/PlGF ratio at birth (p = 0.04). Fetal APOL1 high-risk genotype increases the risk for preeclampsia, likely by adversely affecting placental function. Further research is needed to assess whether APOL1 genetic testing can predict preeclampsia and improve pregnancy outcomes.",
keywords = "APOL1, African American, fetal genotype, health disparity, preeclampsia, prematurity",
author = "Reidy, {Kimberly J.} and Hjorten, {Rebecca C.} and Simpson, {Claire L.} and Rosenberg, {Avi Z.} and Rosenblum, {Stacy D.} and Kovesdy, {Csaba P.} and Tylavsky, {Frances A.} and Joseph Myrie and Ruiz, {Bianca L.} and Soulin Haque and Khyobeni Mozhui and Nelson, {George W.} and David, {Victor A.} and Xiaoping Yang and Masako Suzuki and Jack Jacob and Reznik, {Sandra E.} and Kaskel, {Frederick J.} and Kopp, {Jeffrey B.} and Winkler, {Cheryl A.} and Davis, {Robert L.}",
note = "Funding Information: The authors acknowledge the assistance of Dr. Ellen J. Silver for assistance with statistical analysis of the EMC population data. The project has been supported in part the National Institutes of Health , including the National Institute of Diabetes and Digestive and Kidney Diseases Intramural Research Program (J.B.K.) and the National Cancer Institute Intramural Research Program (C.A.W.) and under contract HHSN26120080001E (C.A.W.). K.J.R. receives support by a Pediatric Young Investigator Award from the Children{\textquoteright}s Hospital at Montefiore & Albert Einstein College of Medicine and was supported by NIH K08 DK091507 and with a catalytic seed grant from the NIH CTSA Grant Number 1 UL1 TR001073 . R.C.H. was supported by NIH T32 DK007110 and is currently supported by NIH T32 DK007695-16 . The CANDLE study was supported by the University of Tennessee Health Science Center{\textquoteright}s Clinical Translational Science Institute and by grants from the Urban Child Institute, Memphis, TN . The content of this publication does not necessarily reflect the view or policy of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the government. A portion of this work was presented at the American Society of Nephrology Kidney Week (2016), Pediatric Academic Societies annual meeting (2017), and the ISSHP European Congress (2017). Publisher Copyright: {\textcopyright} 2018 The Author(s)",
year = "2018",
month = sep,
day = "6",
doi = "10.1016/j.ajhg.2018.08.002",
language = "English (US)",
volume = "103",
pages = "367--376",
journal = "American Journal of Human Genetics",
issn = "0002-9297",
publisher = "Cell Press",
number = "3",
}
