[Anemia as a risk factor for CKD and CVD].
Identifieur interne : 000210 ( Main/Exploration ); précédent : 000209; suivant : 000211[Anemia as a risk factor for CKD and CVD].
Auteurs : Kazuhiko Tsuruya [Japon] ; Hideki HirakataSource :
- Nihon rinsho. Japanese journal of clinical medicine [ 0047-1852 ] ; 2008.
Descripteurs français
- KwdFr :
- Antianémiques (usage thérapeutique), Anémie (complications), Anémie (sang), Anémie (traitement médicamenteux), Défaillance rénale chronique (prévention et contrôle), Défaillance rénale chronique (étiologie), Essais contrôlés randomisés comme sujet (MeSH), Facteurs de risque (MeSH), Humains (MeSH), Hémoglobines (métabolisme), Maladie chronique (MeSH), Maladies cardiovasculaires (prévention et contrôle), Maladies cardiovasculaires (étiologie), Maladies du rein (prévention et contrôle), Maladies du rein (étiologie), Pronostic (MeSH), Protéines recombinantes (MeSH), Syndrome (MeSH), Érythropoïétine (usage thérapeutique), Évolution de la maladie (MeSH).
- MESH :
- métabolisme : Anémie, Hémoglobines.
- prévention et contrôle : Défaillance rénale chronique, Maladies cardiovasculaires, Maladies du rein.
- sang : Anémie.
- traitement médicamenteux : Anémie.
- usage thérapeutique : Antianémiques, Érythropoïétine.
- étiologie : Défaillance rénale chronique, Maladies cardiovasculaires, Maladies du rein.
- Essais contrôlés randomisés comme sujet, Facteurs de risque, Humains, Maladie chronique, Pronostic, Protéines recombinantes, Syndrome, Évolution de la maladie.
English descriptors
- KwdEn :
- Anemia (blood), Anemia (complications), Anemia (drug therapy), Cardiovascular Diseases (etiology), Cardiovascular Diseases (prevention & control), Chronic Disease (MeSH), Disease Progression (MeSH), Erythropoietin (therapeutic use), Hematinics (therapeutic use), Hemoglobins (metabolism), Humans (MeSH), Kidney Diseases (etiology), Kidney Diseases (prevention & control), Kidney Failure, Chronic (etiology), Kidney Failure, Chronic (prevention & control), Prognosis (MeSH), Randomized Controlled Trials as Topic (MeSH), Recombinant Proteins (MeSH), Risk Factors (MeSH), Syndrome (MeSH).
- MESH :
- chemical , metabolism : Hemoglobins.
- chemical , therapeutic use : Erythropoietin, Hematinics.
- blood : Anemia.
- complications : Anemia.
- drug therapy : Anemia.
- etiology : Cardiovascular Diseases, Kidney Diseases, Kidney Failure, Chronic.
- prevention & control : Cardiovascular Diseases, Kidney Diseases, Kidney Failure, Chronic.
- Chronic Disease, Disease Progression, Humans, Prognosis, Randomized Controlled Trials as Topic, Recombinant Proteins, Risk Factors, Syndrome.
Abstract
Chronic kidney disease (CKD) is now recognized as a risk factor of both end-stage renal disease (ESRD) and independently cardiovascular disease (CVD). Therefore, a specific renoprotective intervention is strongly recommended, including blood pressure control as well as anemia improvement with erythropoietin stimulating agents (ESAs). Treatment of renal anemia with ESAs has been proved to improve quality of life (QOL) and finally reduce patient mortality. Recently, Silverberg, et al. created a novel clinical entity of Cardio-Renal Anemia (CRA) syndrome, in which anemia plays a key role for worsening both CKD and cardiac performance in a vicious circle. An appropriate and vigorous treatment of anemia has now been accepted to terminate or weaken the circle. Recently, two large-scaled randomized controlled trials were reported, being the CREATE (cardiovascular risk reduction by early anemia treatment with epoetin beta) study and the CHOIR (correction of hemoglobin and outcomes in renal insufficiency) study. They demonstrated that early initiation of ESA treatment and targeting at higher hemoglobin level (near normal level) failed to show the lowering effects for cardiovascular events as compared to a group in which Hb targeting was lower (sub-normal level) in pre-dialysis CKD patients. While there has been many argues in these reports especially about baseline patients characteristics, being a quite high incidence of severe cardiovascular co-morbidity. Thus, further evidences should be accumulated to resolve a proper target level of Hb in ESA treatment.
PubMed: 18788410
Affiliations:
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Therefore, a specific renoprotective intervention is strongly recommended, including blood pressure control as well as anemia improvement with erythropoietin stimulating agents (ESAs). Treatment of renal anemia with ESAs has been proved to improve quality of life (QOL) and finally reduce patient mortality. Recently, Silverberg, et al. created a novel clinical entity of Cardio-Renal Anemia (CRA) syndrome, in which anemia plays a key role for worsening both CKD and cardiac performance in a vicious circle. An appropriate and vigorous treatment of anemia has now been accepted to terminate or weaken the circle. Recently, two large-scaled randomized controlled trials were reported, being the CREATE (cardiovascular risk reduction by early anemia treatment with epoetin beta) study and the CHOIR (correction of hemoglobin and outcomes in renal insufficiency) study. They demonstrated that early initiation of ESA treatment and targeting at higher hemoglobin level (near normal level) failed to show the lowering effects for cardiovascular events as compared to a group in which Hb targeting was lower (sub-normal level) in pre-dialysis CKD patients. While there has been many argues in these reports especially about baseline patients characteristics, being a quite high incidence of severe cardiovascular co-morbidity. Thus, further evidences should be accumulated to resolve a proper target level of Hb in ESA treatment.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18788410</PMID><DateCompleted><Year>2008</Year><Month>10</Month><Day>16</Day></DateCompleted><DateRevised><Year>2011</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0047-1852</ISSN><JournalIssue CitedMedium="Print"><Volume>66</Volume><Issue>9</Issue><PubDate><Year>2008</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Nihon rinsho. Japanese journal of clinical medicine</Title></Journal><ArticleTitle>[Anemia as a risk factor for CKD and CVD].</ArticleTitle><Pagination><MedlinePgn>1786-93</MedlinePgn></Pagination><Abstract><AbstractText>Chronic kidney disease (CKD) is now recognized as a risk factor of both end-stage renal disease (ESRD) and independently cardiovascular disease (CVD). Therefore, a specific renoprotective intervention is strongly recommended, including blood pressure control as well as anemia improvement with erythropoietin stimulating agents (ESAs). Treatment of renal anemia with ESAs has been proved to improve quality of life (QOL) and finally reduce patient mortality. Recently, Silverberg, et al. created a novel clinical entity of Cardio-Renal Anemia (CRA) syndrome, in which anemia plays a key role for worsening both CKD and cardiac performance in a vicious circle. An appropriate and vigorous treatment of anemia has now been accepted to terminate or weaken the circle. Recently, two large-scaled randomized controlled trials were reported, being the CREATE (cardiovascular risk reduction by early anemia treatment with epoetin beta) study and the CHOIR (correction of hemoglobin and outcomes in renal insufficiency) study. They demonstrated that early initiation of ESA treatment and targeting at higher hemoglobin level (near normal level) failed to show the lowering effects for cardiovascular events as compared to a group in which Hb targeting was lower (sub-normal level) in pre-dialysis CKD patients. While there has been many argues in these reports especially about baseline patients characteristics, being a quite high incidence of severe cardiovascular co-morbidity. Thus, further evidences should be accumulated to resolve a proper target level of Hb in ESA treatment.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tsuruya</LastName><ForeName>Kazuhiko</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Integrated Therapy for Chronic Kidney Disease, Graduate School of Medical Sciences, Kyushu University.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hirakata</LastName><ForeName>Hideki</ForeName><Initials>H</Initials></Author></AuthorList><Language>jpn</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>Nihon Rinsho</MedlineTA><NlmUniqueID>0420546</NlmUniqueID><ISSNLinking>0047-1852</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006397">Hematinics</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006454">Hemoglobins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011994">Recombinant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C103998">epoetin beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>11096-26-7</RegistryNumber><NameOfSubstance UI="D004921">Erythropoietin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000740" MajorTopicYN="N">Anemia</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002908" MajorTopicYN="N">Chronic Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004921" MajorTopicYN="N">Erythropoietin</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006397" MajorTopicYN="N">Hematinics</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006454" MajorTopicYN="N">Hemoglobins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007674" MajorTopicYN="N">Kidney Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007676" MajorTopicYN="N">Kidney Failure, Chronic</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016032" MajorTopicYN="N">Randomized Controlled Trials as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011994" MajorTopicYN="N">Recombinant Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013577" MajorTopicYN="N">Syndrome</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>28</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>9</Month><Day>16</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>10</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>9</Month><Day>16</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18788410</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country><region><li>Kyūshū</li><li>Préfecture de Fukuoka</li></region><settlement><li>Fukuoka</li></settlement><orgName><li>Université de Kyūshū</li></orgName></list><tree><noCountry><name sortKey="Hirakata, Hideki" sort="Hirakata, Hideki" uniqKey="Hirakata H" first="Hideki" last="Hirakata">Hideki Hirakata</name></noCountry><country name="Japon"><region name="Kyūshū"><name sortKey="Tsuruya, Kazuhiko" sort="Tsuruya, Kazuhiko" uniqKey="Tsuruya K" first="Kazuhiko" last="Tsuruya">Kazuhiko Tsuruya</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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