Urinary Excretion of C5b-9 is Associated With the Anti-Angiogenic State in Severe Preeclampsia
Problem Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and angiogenic factors in human pregnancy is unclear. Method of study Utilizing existing biomarkers, our study sought to better understand this...
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| Published in | American journal of reproductive immunology (1989) Vol. 73; no. 5; pp. 437 - 444 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Denmark
Blackwell Publishing Ltd
01.05.2015
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1046-7408 1600-0897 1600-0897 |
| DOI | 10.1111/aji.12349 |
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| Abstract | Problem
Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and angiogenic factors in human pregnancy is unclear.
Method of study
Utilizing existing biomarkers, our study sought to better understand this relationship in active disease. We performed a case–control study, enrolling 25 cases with severe preeclampsia, 25 controls with chronic hypertension, and 25 healthy controls without hypertension. Levels of complement components (C3a, C5a, and C5b‐9) and angiogenic markers [basic fibroblast growth factor (bFGF), placental growth factor (PlGF), vascular endothelial growth factor (VEGF), and soluble fms‐like tyrosine kinase‐1 (sFlt‐1)] were measured simultaneously.
Results
Compared to both hypertensive and non‐hypertensive controls, severe preeclampsia was associated with increased plasma sFlt‐1, decreased plasma VEGF and PlGF, decreased urinary PlGF, and increased urinary C5b‐9. Urinary marker C5b‐9 correlated strongly with the anti‐angiogenic condition. In subjects with detectable urinary excretion of C5b‐9, median plasma levels of sFlt‐1 were significantly greater (32,029 versus 4556 pg/mL, P < 0.0001) and levels of PlGF (15.6 versus 226 pg/mL, P < 0.0001) and VEGF (119 versus 153 pg/mL, P = 0.001) were significantly lower.
Conclusion
More so than plasma complement markers, urinary C5b‐9 may a useful measure to link complement dysregulation with angiogenic imbalance in severe preeclampsia. |
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| AbstractList | Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and angiogenic factors in human pregnancy is unclear.
Utilizing existing biomarkers, our study sought to better understand this relationship in active disease. We performed a case-control study, enrolling 25 cases with severe preeclampsia, 25 controls with chronic hypertension, and 25 healthy controls without hypertension. Levels of complement components (C3a, C5a, and C5b-9) and angiogenic markers [basic fibroblast growth factor (bFGF), placental growth factor (PlGF), vascular endothelial growth factor (VEGF), and soluble fms-like tyrosine kinase-1 (sFlt-1)] were measured simultaneously.
Compared to both hypertensive and non-hypertensive controls, severe preeclampsia was associated with increased plasma sFlt-1, decreased plasma VEGF and PlGF, decreased urinary PlGF, and increased urinary C5b-9. Urinary marker C5b-9 correlated strongly with the anti-angiogenic condition. In subjects with detectable urinary excretion of C5b-9, median plasma levels of sFlt-1 were significantly greater (32,029 versus 4556 pg/mL, P < 0.0001) and levels of PlGF (15.6 versus 226 pg/mL, P < 0.0001) and VEGF (119 versus 153 pg/mL, P = 0.001) were significantly lower.
More so than plasma complement markers, urinary C5b-9 may a useful measure to link complement dysregulation with angiogenic imbalance in severe preeclampsia. Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and angiogenic factors in human pregnancy is unclear.PROBLEMSevere preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and angiogenic factors in human pregnancy is unclear.Utilizing existing biomarkers, our study sought to better understand this relationship in active disease. We performed a case-control study, enrolling 25 cases with severe preeclampsia, 25 controls with chronic hypertension, and 25 healthy controls without hypertension. Levels of complement components (C3a, C5a, and C5b-9) and angiogenic markers [basic fibroblast growth factor (bFGF), placental growth factor (PlGF), vascular endothelial growth factor (VEGF), and soluble fms-like tyrosine kinase-1 (sFlt-1)] were measured simultaneously.METHOD OF STUDYUtilizing existing biomarkers, our study sought to better understand this relationship in active disease. We performed a case-control study, enrolling 25 cases with severe preeclampsia, 25 controls with chronic hypertension, and 25 healthy controls without hypertension. Levels of complement components (C3a, C5a, and C5b-9) and angiogenic markers [basic fibroblast growth factor (bFGF), placental growth factor (PlGF), vascular endothelial growth factor (VEGF), and soluble fms-like tyrosine kinase-1 (sFlt-1)] were measured simultaneously.Compared to both hypertensive and non-hypertensive controls, severe preeclampsia was associated with increased plasma sFlt-1, decreased plasma VEGF and PlGF, decreased urinary PlGF, and increased urinary C5b-9. Urinary marker C5b-9 correlated strongly with the anti-angiogenic condition. In subjects with detectable urinary excretion of C5b-9, median plasma levels of sFlt-1 were significantly greater (32,029 versus 4556 pg/mL, P < 0.0001) and levels of PlGF (15.6 versus 226 pg/mL, P < 0.0001) and VEGF (119 versus 153 pg/mL, P = 0.001) were significantly lower.RESULTSCompared to both hypertensive and non-hypertensive controls, severe preeclampsia was associated with increased plasma sFlt-1, decreased plasma VEGF and PlGF, decreased urinary PlGF, and increased urinary C5b-9. Urinary marker C5b-9 correlated strongly with the anti-angiogenic condition. In subjects with detectable urinary excretion of C5b-9, median plasma levels of sFlt-1 were significantly greater (32,029 versus 4556 pg/mL, P < 0.0001) and levels of PlGF (15.6 versus 226 pg/mL, P < 0.0001) and VEGF (119 versus 153 pg/mL, P = 0.001) were significantly lower.More so than plasma complement markers, urinary C5b-9 may a useful measure to link complement dysregulation with angiogenic imbalance in severe preeclampsia.CONCLUSIONMore so than plasma complement markers, urinary C5b-9 may a useful measure to link complement dysregulation with angiogenic imbalance in severe preeclampsia. Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and angiogenic factors in human pregnancy is unclear. Utilizing existing biomarkers, our study sought to better understand this relationship in active disease. We performed a case-control study, enrolling 25 cases with severe preeclampsia, 25 controls with chronic hypertension, and 25 healthy controls without hypertension. Levels of complement components (C3a, C5a, and C5b-9) and angiogenic markers [basic fibroblast growth factor (bFGF), placental growth factor (PlGF), vascular endothelial growth factor (VEGF), and soluble fms-like tyrosine kinase-1 (sFlt-1)] were measured simultaneously. Compared to both hypertensive and non-hypertensive controls, severe preeclampsia was associated with increased plasma sFlt-1, decreased plasma VEGF and PlGF, decreased urinary PlGF, and increased urinary C5b-9. Urinary marker C5b-9 correlated strongly with the anti-angiogenic condition. In subjects with detectable urinary excretion of C5b-9, median plasma levels of sFlt-1 were significantly greater (32,029 versus 4556 pg/mL, P < 0.0001) and levels of PlGF (15.6 versus 226 pg/mL, P < 0.0001) and VEGF (119 versus 153 pg/mL, P = 0.001) were significantly lower. More so than plasma complement markers, urinary C5b-9 may a useful measure to link complement dysregulation with angiogenic imbalance in severe preeclampsia. Problem Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and angiogenic factors in human pregnancy is unclear. Method of study Utilizing existing biomarkers, our study sought to better understand this relationship in active disease. We performed a case-control study, enrolling 25 cases with severe preeclampsia, 25 controls with chronic hypertension, and 25 healthy controls without hypertension. Levels of complement components (C3a, C5a, and C5b-9) and angiogenic markers [basic fibroblast growth factor (bFGF), placental growth factor (PlGF), vascular endothelial growth factor (VEGF), and soluble fms-like tyrosine kinase-1 (sFlt-1)] were measured simultaneously. Results Compared to both hypertensive and non-hypertensive controls, severe preeclampsia was associated with increased plasma sFlt-1, decreased plasma VEGF and PlGF, decreased urinary PlGF, and increased urinary C5b-9. Urinary marker C5b-9 correlated strongly with the anti-angiogenic condition. In subjects with detectable urinary excretion of C5b-9, median plasma levels of sFlt-1 were significantly greater (32,029 versus 4556 pg/mL, P < 0.0001) and levels of PlGF (15.6 versus 226 pg/mL, P < 0.0001) and VEGF (119 versus 153 pg/mL, P = 0.001) were significantly lower. Conclusion More so than plasma complement markers, urinary C5b-9 may a useful measure to link complement dysregulation with angiogenic imbalance in severe preeclampsia. Problem Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and angiogenic factors in human pregnancy is unclear. Method of study Utilizing existing biomarkers, our study sought to better understand this relationship in active disease. We performed a case–control study, enrolling 25 cases with severe preeclampsia, 25 controls with chronic hypertension, and 25 healthy controls without hypertension. Levels of complement components (C3a, C5a, and C5b‐9) and angiogenic markers [basic fibroblast growth factor (bFGF), placental growth factor (PlGF), vascular endothelial growth factor (VEGF), and soluble fms‐like tyrosine kinase‐1 (sFlt‐1)] were measured simultaneously. Results Compared to both hypertensive and non‐hypertensive controls, severe preeclampsia was associated with increased plasma sFlt‐1, decreased plasma VEGF and PlGF, decreased urinary PlGF, and increased urinary C5b‐9. Urinary marker C5b‐9 correlated strongly with the anti‐angiogenic condition. In subjects with detectable urinary excretion of C5b‐9, median plasma levels of sFlt‐1 were significantly greater (32,029 versus 4556 pg/mL, P < 0.0001) and levels of PlGF (15.6 versus 226 pg/mL, P < 0.0001) and VEGF (119 versus 153 pg/mL, P = 0.001) were significantly lower. Conclusion More so than plasma complement markers, urinary C5b‐9 may a useful measure to link complement dysregulation with angiogenic imbalance in severe preeclampsia. |
| Author | Feinberg, Bruce B. Dawood, Hassan Y. Guseh, Stephanie H. Burwick, Richard M. Yamamoto, Hidemi S. Fichorova, Raina N. |
| Author_xml | – sequence: 1 givenname: Stephanie H. surname: Guseh fullname: Guseh, Stephanie H. organization: Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women's Hospital, Harvard Medical School, MA, Boston, USA – sequence: 2 givenname: Bruce B. surname: Feinberg fullname: Feinberg, Bruce B. organization: Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Columbia University Medical Center, NY, New York, USA – sequence: 3 givenname: Hassan Y. surname: Dawood fullname: Dawood, Hassan Y. organization: Department of Obstetrics, Gynecology and Reproductive Biology, Laboratory of Genital Tract Biology, Brigham and Women's Hospital, Harvard Medical School, MA, Boston, USA – sequence: 4 givenname: Hidemi S. surname: Yamamoto fullname: Yamamoto, Hidemi S. organization: Department of Obstetrics, Gynecology and Reproductive Biology, Laboratory of Genital Tract Biology, Brigham and Women's Hospital, Harvard Medical School, MA, Boston, USA – sequence: 5 givenname: Raina N. surname: Fichorova fullname: Fichorova, Raina N. organization: Department of Obstetrics, Gynecology and Reproductive Biology, Laboratory of Genital Tract Biology, Brigham and Women's Hospital, Harvard Medical School, MA, Boston, USA – sequence: 6 givenname: Richard M. surname: Burwick fullname: Burwick, Richard M. email: Richard M. Burwick, Division of Maternal Fetal Medicine, Oregon Health and Science University, Mail Code: L-458, 3181 SW Sam Jackson Park Road, Portland, OR 97239-3098, USA. , burwick@ohsu.edu organization: Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Oregon Health and Science University, OR, Portland, USA |
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| Keywords | Angiogenic proteins complement system proteins preeclampsia C5b-9 |
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| Notes | Figure S1. Urinary concentration of angiogenic factors normalized to creatinine in healthy controls, chronic hypertension, and severe preeclampsia.Table S1. Characteristics of study subjects by group.Table S2. Correlations between plasma angiogenic factors and plasma complement components in severe preeclampsia (n = 25).Table S3. Correlations between urinary angiogenic factors and urinary complement components in severe preeclampsia (n = 25). istex:8EDE345855E017E3CDA30547BA7F05E6399B0D7E ArticleID:AJI12349 ark:/67375/WNG-WLZ1PC2W-9 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23 |
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ACOG practice bulletin (e_1_2_9_31_1) 2002; 99 e_1_2_9_2_1 e_1_2_9_26_1 e_1_2_9_49_1 e_1_2_9_28_1 e_1_2_9_47_1 e_1_2_9_30_1 e_1_2_9_11_1 e_1_2_9_34_1 e_1_2_9_13_1 e_1_2_9_32_1 e_1_2_9_15_1 e_1_2_9_38_1 e_1_2_9_36_1 e_1_2_9_19_1 Messias‐Reason IJ (e_1_2_9_17_1) 2000; 10 e_1_2_9_40_1 e_1_2_9_21_1 e_1_2_9_46_1 e_1_2_9_23_1 e_1_2_9_44_1 Kerjaschki D (e_1_2_9_43_1) 1989; 143 e_1_2_9_7_1 e_1_2_9_5_1 e_1_2_9_3_1 Oppermann M (e_1_2_9_42_1) 1994; 82 e_1_2_9_9_1 e_1_2_9_25_1 e_1_2_9_27_1 e_1_2_9_48_1 e_1_2_9_29_1 |
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Ultrasound Obstet Gynecol 2007; 29:407-413. – volume: 117 start-page: 75 year: 2011 end-page: 83 article-title: Early elevations of the complement activation fragment C3a and adverse pregnancy outcomes publication-title: Obstet Gynecol – volume: 47 start-page: 1403 year: 1995 end-page: 1411 article-title: Urinary excretion of protectin (CD59), complement SC5b‐9 and cytokines in membranous glomerulonephritis publication-title: Kidney Int – volume: 116 start-page: 4395 year: 2010 end-page: 4403 article-title: Complement‐mediated inhibition of neovascularization reveals a point of convergence between innate immunity and angiogenesis publication-title: Blood – volume: 121 start-page: 14 issue: Suppl. 1 year: 2014 end-page: 24 article-title: Pre‐eclampsia, eclampsia and adverse maternal and perinatal outcomes: a secondary analysis of the World Health Organization Multicountry Survey on Maternal and Newborn Health publication-title: BJOG – volume: 27 start-page: 55 year: 2012 end-page: 58 article-title: Pitfalls in urinary complement measurements publication-title: Transpl Immunol – volume: 111 start-page: 624 year: 2008 end-page: 632 article-title: Membrane cofactor protein mutations in atypical hemolytic uremic syndrome (aHUS), fatal Stx‐HUS, C3 glomerulonephritis, and the HELLP syndrome publication-title: Blood – volume: 33 start-page: 143 year: 2012 end-page: 150 article-title: The characterization of fibrocyte‐like cells: a novel fibroblastic cell of the placenta publication-title: Placenta – volume: 13 start-page: 215 year: 2013 end-page: 226 article-title: Complement activation and the resulting placental vascular insufficiency drives fetal growth restriction associated with placental malaria publication-title: Cell Host Microbe – volume: 367 start-page: 1066 year: 2006 end-page: 1074 article-title: WHO analysis of causes of maternal death: a systematic review publication-title: Lancet – volume: 56 start-page: 91 year: 2013 end-page: 97 article-title: Complement activation is critical for placental ischemia‐induced hypertension in the rat publication-title: Mol Immunol – volume: 111 start-page: 649 year: 2003 end-page: 658 article-title: Excess placental soluble fms‐like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia publication-title: J Clin Invest – volume: 68 start-page: 258 year: 2012 end-page: 270 article-title: Biomarkers of coagulation, inflammation, and angiogenesis are independently associated with preeclampsia publication-title: Am J Reprod Immunol – volume: 12 start-page: 682 year: 2006 end-page: 687 article-title: Generation of C5a in the absence of C3: a new complement activation pathway publication-title: Nat Med – volume: 121 start-page: 78 year: 2013 end-page: 81 article-title: Errors in the treatment of hypertensive disorders of pregnancy and their impact on maternal mortality publication-title: Int J Gynaecol Obstet – volume: 11 start-page: 700 year: 2000 end-page: 707 article-title: Complement activation products in the urine from proteinuric patients publication-title: J Am Soc Nephrol – volume: 87 start-page: 837 year: 2008 end-page: 842 article-title: Endoglin, PlGF and sFlt‐1 as markers of predicting preeclampsia publication-title: Acta Obstet Gynecol Scand – volume: 60 start-page: 712 year: 2012 end-page: 721 article-title: Autoantibody‐mediated complement C3a receptor activation contributes to the pathogenesis of preeclampsia publication-title: Hypertension – volume: 99 start-page: 159 year: 2002 end-page: 167 article-title: Diagnosis and management of preeclampsia and eclampsia. 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Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement... Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement and... Problem Severe preeclampsia has been independently linked to complement dysregulation and angiogenic imbalance; however, the relationship between complement... |
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| SubjectTerms | Adult Angiogenic proteins Biomarkers - urine C5b-9 Case-Control Studies Complement Membrane Attack Complex - urine complement system proteins Female Fibroblast Growth Factor 2 - urine Follow-Up Studies Humans Placenta Growth Factor Pre-Eclampsia - urine preeclampsia Pregnancy Pregnancy Proteins - urine Vascular Endothelial Growth Factor A - urine Vascular Endothelial Growth Factor Receptor-1 - urine |
| Title | Urinary Excretion of C5b-9 is Associated With the Anti-Angiogenic State in Severe Preeclampsia |
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