Impact of pre‐eclampsia on renal outcome in sickle cell disease patients

Summary The long‐term consequences of pre‐eclampsia (PrE) for renal function have never been determined in patients with sickle cell disease (SCD). Between 2008 and 2015, we screened 306 pregnancies in women with SCD and identified 40 with PrE (13%). The control group consisted of 65 pregnant SCD pa...

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Veröffentlicht in:British journal of haematology 2021-09, Vol.194 (6), p.1053-1062
Hauptverfasser: Boudhabhay, Idris, Boutin, Emmanuelle, Bartolucci, Pablo, Bornes, Marie‐Isabelle, Habibi, Anoosha, Lionnet, François, Hertig, Alexandre, Grimbert, Philippe, Stehlé, Thomas, El Karoui, Khalil, Sahali, Dil, Fois, Elena, Rémy, Philippe, Galacteros, Frédéric, Haddad, Bassam, Canoui-Poitrine, Florence, Lecarpentier, Edouard, Audard, Vincent
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container_issue 6
container_start_page 1053
container_title British journal of haematology
container_volume 194
creator Boudhabhay, Idris
Boutin, Emmanuelle
Bartolucci, Pablo
Bornes, Marie‐Isabelle
Habibi, Anoosha
Lionnet, François
Hertig, Alexandre
Grimbert, Philippe
Stehlé, Thomas
El Karoui, Khalil
Sahali, Dil
Fois, Elena
Rémy, Philippe
Galacteros, Frédéric
Haddad, Bassam
Canoui-Poitrine, Florence
Lecarpentier, Edouard
Audard, Vincent
description Summary The long‐term consequences of pre‐eclampsia (PrE) for renal function have never been determined in patients with sickle cell disease (SCD). Between 2008 and 2015, we screened 306 pregnancies in women with SCD and identified 40 with PrE (13%). The control group consisted of 65 pregnant SCD patients without PrE. In multivariable analysis, PrE events were associated with an increase of 1 log of lactate dehydrogenase level (adjusted odds ratio, aOR = 3·83, P = 0·05), a decrease of 10 g/l of haemoglobin levels (aOR = 2·48, P = 0·006) and one or more vaso‐occlusive crisis during pregnancy (aOR = 16·68, P = 0·002). Estimated glomerular filtration rate (eGFR) was similar in the two groups at steady state but was significantly lower in the PrE group after one year of follow‐up and at last follow‐up (130 vs 148 ml/min/1·73 m2, P 
doi_str_mv 10.1111/bjh.17606
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Between 2008 and 2015, we screened 306 pregnancies in women with SCD and identified 40 with PrE (13%). The control group consisted of 65 pregnant SCD patients without PrE. In multivariable analysis, PrE events were associated with an increase of 1 log of lactate dehydrogenase level (adjusted odds ratio, aOR = 3·83, P = 0·05), a decrease of 10 g/l of haemoglobin levels (aOR = 2·48, P = 0·006) and one or more vaso‐occlusive crisis during pregnancy (aOR = 16·68, P = 0·002). Estimated glomerular filtration rate (eGFR) was similar in the two groups at steady state but was significantly lower in the PrE group after one year of follow‐up and at last follow‐up (130 vs 148 ml/min/1·73 m2, P &lt; 0·001 and 120 vs 130 ml/min/1·73 m2, P &lt; 0·001, respectively). In multivariable analysis, eGFR had returned to steady‐state levels one year after pregnancy in patients without PrE but continued to decrease in patients with PrE (β = −18·15 ml/min/1·73 m2, P &lt; 0·001). This decline was more marked at the end of follow‐up (β = −31·15 ml/min, P &lt; 0·001). 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Between 2008 and 2015, we screened 306 pregnancies in women with SCD and identified 40 with PrE (13%). The control group consisted of 65 pregnant SCD patients without PrE. In multivariable analysis, PrE events were associated with an increase of 1 log of lactate dehydrogenase level (adjusted odds ratio, aOR = 3·83, P = 0·05), a decrease of 10 g/l of haemoglobin levels (aOR = 2·48, P = 0·006) and one or more vaso‐occlusive crisis during pregnancy (aOR = 16·68, P = 0·002). Estimated glomerular filtration rate (eGFR) was similar in the two groups at steady state but was significantly lower in the PrE group after one year of follow‐up and at last follow‐up (130 vs 148 ml/min/1·73 m2, P &lt; 0·001 and 120 vs 130 ml/min/1·73 m2, P &lt; 0·001, respectively). In multivariable analysis, eGFR had returned to steady‐state levels one year after pregnancy in patients without PrE but continued to decrease in patients with PrE (β = −18·15 ml/min/1·73 m2, P &lt; 0·001). This decline was more marked at the end of follow‐up (β = −31·15 ml/min, P &lt; 0·001). In conclusion, PrE episodes are associated with a significant risk of subsequent renal function decline in SCD patients.</description><subject>Adult</subject><subject>Anemia, Sickle Cell - complications</subject><subject>Anemia, Sickle Cell - physiopathology</subject><subject>chronic kidney disease</subject><subject>Eclampsia</subject><subject>Epidermal growth factor receptors</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Glomerular Filtration Rate</subject><subject>Hematology</subject><subject>Hemoglobin</subject><subject>Humans</subject><subject>Kidney - physiopathology</subject><subject>Kidney Diseases - etiology</subject><subject>Kidney Diseases - physiopathology</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactic acid</subject><subject>Life Sciences</subject><subject>Pre-Eclampsia - physiopathology</subject><subject>Preeclampsia</subject><subject>Pregnancy</subject><subject>pre‐eclampsia</subject><subject>Renal function</subject><subject>risk factors</subject><subject>Santé publique et épidémiologie</subject><subject>Sickle cell anemia</subject><subject>Sickle cell disease</subject><subject>sickle cell nephropathy</subject><issn>0007-1048</issn><issn>1365-2141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9K5EAQxhtZ0Vn14AtIw17cQ7Qr_S85qqyOMuBFz02nU8Eek3RMJ4q3fYR9xn0SM46KCNaloPjx1Vf1EbIP7AimOi6Wd0egFVMbZAZcySQFAT_IjDGmE2Ai2yY_Y1wyBpxJ2CLbXACHLOczcnXZdNYNNFS06_H_33_oatt00VsaWtpja2saxsGFBqlvafTuvkbqsK5p6SPaiLSzg8d2iLtks7J1xL23vkNuz__cnM2TxfXF5dnJInEiTVVSYG7TQuVaZdoKYCUiR2SQW-4yi1VpC1AoldRMFBIrdBkIKYUrVZVilvId8nute2dr0_W-sf2zCdab-cnCrGZMgBQik48wsYdrtuvDw4hxMI2PK_e2xTBGk0oBOtNS6gn99QVdhrGf7l9ROs0nC_zTcteHGHusPhwAM6swzBSGeQ1jYg_eFMeiwfKDfP_-BByvgSdf4_P3Sub0ar6WfAFvXZIw</recordid><startdate>202109</startdate><enddate>202109</enddate><creator>Boudhabhay, Idris</creator><creator>Boutin, Emmanuelle</creator><creator>Bartolucci, Pablo</creator><creator>Bornes, Marie‐Isabelle</creator><creator>Habibi, Anoosha</creator><creator>Lionnet, François</creator><creator>Hertig, Alexandre</creator><creator>Grimbert, Philippe</creator><creator>Stehlé, Thomas</creator><creator>El Karoui, Khalil</creator><creator>Sahali, Dil</creator><creator>Fois, Elena</creator><creator>Rémy, Philippe</creator><creator>Galacteros, Frédéric</creator><creator>Haddad, Bassam</creator><creator>Canoui-Poitrine, Florence</creator><creator>Lecarpentier, Edouard</creator><creator>Audard, Vincent</creator><general>Blackwell Publishing Ltd</general><general>Wiley</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0001-5343-2550</orcidid><orcidid>https://orcid.org/0000-0001-9970-6051</orcidid></search><sort><creationdate>202109</creationdate><title>Impact of pre‐eclampsia on renal outcome in sickle cell disease patients</title><author>Boudhabhay, Idris ; Boutin, Emmanuelle ; Bartolucci, Pablo ; Bornes, Marie‐Isabelle ; Habibi, Anoosha ; Lionnet, François ; Hertig, Alexandre ; Grimbert, Philippe ; Stehlé, Thomas ; El Karoui, Khalil ; Sahali, Dil ; Fois, Elena ; Rémy, Philippe ; Galacteros, Frédéric ; Haddad, Bassam ; Canoui-Poitrine, Florence ; Lecarpentier, Edouard ; Audard, Vincent</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4226-be9a2b697687a410dee3ee019a3c8aefdab16e565704b5efec814554cd6f2e823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adult</topic><topic>Anemia, Sickle Cell - complications</topic><topic>Anemia, Sickle Cell - physiopathology</topic><topic>chronic kidney disease</topic><topic>Eclampsia</topic><topic>Epidermal growth factor receptors</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Glomerular Filtration Rate</topic><topic>Hematology</topic><topic>Hemoglobin</topic><topic>Humans</topic><topic>Kidney - physiopathology</topic><topic>Kidney Diseases - etiology</topic><topic>Kidney Diseases - physiopathology</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactic acid</topic><topic>Life Sciences</topic><topic>Pre-Eclampsia - physiopathology</topic><topic>Preeclampsia</topic><topic>Pregnancy</topic><topic>pre‐eclampsia</topic><topic>Renal function</topic><topic>risk factors</topic><topic>Santé publique et épidémiologie</topic><topic>Sickle cell anemia</topic><topic>Sickle cell disease</topic><topic>sickle cell nephropathy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boudhabhay, Idris</creatorcontrib><creatorcontrib>Boutin, Emmanuelle</creatorcontrib><creatorcontrib>Bartolucci, Pablo</creatorcontrib><creatorcontrib>Bornes, Marie‐Isabelle</creatorcontrib><creatorcontrib>Habibi, Anoosha</creatorcontrib><creatorcontrib>Lionnet, François</creatorcontrib><creatorcontrib>Hertig, Alexandre</creatorcontrib><creatorcontrib>Grimbert, Philippe</creatorcontrib><creatorcontrib>Stehlé, Thomas</creatorcontrib><creatorcontrib>El Karoui, Khalil</creatorcontrib><creatorcontrib>Sahali, Dil</creatorcontrib><creatorcontrib>Fois, Elena</creatorcontrib><creatorcontrib>Rémy, Philippe</creatorcontrib><creatorcontrib>Galacteros, Frédéric</creatorcontrib><creatorcontrib>Haddad, Bassam</creatorcontrib><creatorcontrib>Canoui-Poitrine, Florence</creatorcontrib><creatorcontrib>Lecarpentier, Edouard</creatorcontrib><creatorcontrib>Audard, Vincent</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>British journal of haematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boudhabhay, Idris</au><au>Boutin, Emmanuelle</au><au>Bartolucci, Pablo</au><au>Bornes, Marie‐Isabelle</au><au>Habibi, Anoosha</au><au>Lionnet, François</au><au>Hertig, Alexandre</au><au>Grimbert, Philippe</au><au>Stehlé, Thomas</au><au>El Karoui, Khalil</au><au>Sahali, Dil</au><au>Fois, Elena</au><au>Rémy, Philippe</au><au>Galacteros, Frédéric</au><au>Haddad, Bassam</au><au>Canoui-Poitrine, Florence</au><au>Lecarpentier, Edouard</au><au>Audard, Vincent</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of pre‐eclampsia on renal outcome in sickle cell disease patients</atitle><jtitle>British journal of haematology</jtitle><addtitle>Br J Haematol</addtitle><date>2021-09</date><risdate>2021</risdate><volume>194</volume><issue>6</issue><spage>1053</spage><epage>1062</epage><pages>1053-1062</pages><issn>0007-1048</issn><eissn>1365-2141</eissn><abstract>Summary The long‐term consequences of pre‐eclampsia (PrE) for renal function have never been determined in patients with sickle cell disease (SCD). Between 2008 and 2015, we screened 306 pregnancies in women with SCD and identified 40 with PrE (13%). The control group consisted of 65 pregnant SCD patients without PrE. In multivariable analysis, PrE events were associated with an increase of 1 log of lactate dehydrogenase level (adjusted odds ratio, aOR = 3·83, P = 0·05), a decrease of 10 g/l of haemoglobin levels (aOR = 2·48, P = 0·006) and one or more vaso‐occlusive crisis during pregnancy (aOR = 16·68, P = 0·002). Estimated glomerular filtration rate (eGFR) was similar in the two groups at steady state but was significantly lower in the PrE group after one year of follow‐up and at last follow‐up (130 vs 148 ml/min/1·73 m2, P &lt; 0·001 and 120 vs 130 ml/min/1·73 m2, P &lt; 0·001, respectively). In multivariable analysis, eGFR had returned to steady‐state levels one year after pregnancy in patients without PrE but continued to decrease in patients with PrE (β = −18·15 ml/min/1·73 m2, P &lt; 0·001). This decline was more marked at the end of follow‐up (β = −31·15 ml/min, P &lt; 0·001). In conclusion, PrE episodes are associated with a significant risk of subsequent renal function decline in SCD patients.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>34131893</pmid><doi>10.1111/bjh.17606</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-5343-2550</orcidid><orcidid>https://orcid.org/0000-0001-9970-6051</orcidid><oa>free_for_read</oa></addata></record>
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subjects Adult
Anemia, Sickle Cell - complications
Anemia, Sickle Cell - physiopathology
chronic kidney disease
Eclampsia
Epidermal growth factor receptors
Female
Follow-Up Studies
Glomerular Filtration Rate
Hematology
Hemoglobin
Humans
Kidney - physiopathology
Kidney Diseases - etiology
Kidney Diseases - physiopathology
L-Lactate dehydrogenase
Lactic acid
Life Sciences
Pre-Eclampsia - physiopathology
Preeclampsia
Pregnancy
pre‐eclampsia
Renal function
risk factors
Santé publique et épidémiologie
Sickle cell anemia
Sickle cell disease
sickle cell nephropathy
title Impact of pre‐eclampsia on renal outcome in sickle cell disease patients
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