Plasma Lipoprotein(a) Levels and Atherosclerotic Renal Artery Stenosis in Hypertensive Patients
Background/Aims: The contribution of emergent cardiovascular risk factors to atherosclerotic renal artery stenosis (ARAS) is debated. We investigated the relationship of lipoprotein(a) and prothrombotic factors with ARAS in hypertension. Methods: In 50 hypertensive patients with angiographic evidenc...
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| Veröffentlicht in: | Kidney & blood pressure research 2015-01, Vol.40 (2), p.166-175 |
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| creator | Catena, Cristiana Colussi, GianLuca Nait, Francesca Capobianco, Frine Sechi, Leonardo A |
| description | Background/Aims: The contribution of emergent cardiovascular risk factors to atherosclerotic renal artery stenosis (ARAS) is debated. We investigated the relationship of lipoprotein(a) and prothrombotic factors with ARAS in hypertension. Methods: In 50 hypertensive patients with angiographic evidence of ARAS and 58 hypertensive patients who had comparable cardiovascular risk factor burden but no evidence of renovascular disease, we measured renal function, lipoprotein(a), homocysteine, and hemostatic-fibrinolytic markers. Results: Patients with ARAS were more frequently smokers and had longer duration of hypertension, heavier antihypertensive treatment, and worse renal function than controls. Lipoprotein(a) was higher in patients with ARAS than controls, whereas no differences were found in homocysteine and all hemostatic variables. Multivariate analysis showed that lipoprotein(a) was associated with ARAS independent of other confounders including renal function and history of coronary heart, cerebrovascular, and peripheral artery disease. Conclusion: Lipoprotein(a) might contribute to the development of ARAS and detection of elevated levels of this lipoprotein could raise the suspicion of renovascular disease in patients with high blood pressure. |
| doi_str_mv | 10.1159/000368492 |
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We investigated the relationship of lipoprotein(a) and prothrombotic factors with ARAS in hypertension. Methods: In 50 hypertensive patients with angiographic evidence of ARAS and 58 hypertensive patients who had comparable cardiovascular risk factor burden but no evidence of renovascular disease, we measured renal function, lipoprotein(a), homocysteine, and hemostatic-fibrinolytic markers. Results: Patients with ARAS were more frequently smokers and had longer duration of hypertension, heavier antihypertensive treatment, and worse renal function than controls. Lipoprotein(a) was higher in patients with ARAS than controls, whereas no differences were found in homocysteine and all hemostatic variables. Multivariate analysis showed that lipoprotein(a) was associated with ARAS independent of other confounders including renal function and history of coronary heart, cerebrovascular, and peripheral artery disease. Conclusion: Lipoprotein(a) might contribute to the development of ARAS and detection of elevated levels of this lipoprotein could raise the suspicion of renovascular disease in patients with high blood pressure.</description><identifier>ISSN: 1420-4096</identifier><identifier>EISSN: 1423-0143</identifier><identifier>DOI: 10.1159/000368492</identifier><identifier>PMID: 25871336</identifier><identifier>CODEN: RPBIEL</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Aged ; Atherosclerosis - etiology ; Atherosclerosis - pathology ; Complications and side effects ; Cross-Sectional Studies ; Diagnosis ; Female ; Fibrinolysis ; Health aspects ; Hemostasis ; Homocysteine ; Humans ; Hypertension ; Hypertension - complications ; Hypertension - pathology ; Ischemic nephropathy ; Kidney Function Tests ; Lipoprotein A ; Lipoprotein(a) - blood ; Male ; Middle Aged ; Original Paper ; Prothrombotic state ; Renal artery obstruction ; Renal Artery Obstruction - etiology ; Renal Artery Obstruction - pathology ; Renovascular hypertension ; Risk Factors</subject><ispartof>Kidney & blood pressure research, 2015-01, Vol.40 (2), p.166-175</ispartof><rights>2015 S. Karger AG, Basel</rights><rights>2015 S. Karger AG, Basel.</rights><rights>COPYRIGHT 2015 S. Karger AG</rights><rights>Copyright S. Karger AG Apr 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c530t-ce8fade0ab485cab2b3990d5b0688a366ca8c6a832e147be0900d9b9b2753e7f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2100,27633,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25871336$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Catena, Cristiana</creatorcontrib><creatorcontrib>Colussi, GianLuca</creatorcontrib><creatorcontrib>Nait, Francesca</creatorcontrib><creatorcontrib>Capobianco, Frine</creatorcontrib><creatorcontrib>Sechi, Leonardo A</creatorcontrib><title>Plasma Lipoprotein(a) Levels and Atherosclerotic Renal Artery Stenosis in Hypertensive Patients</title><title>Kidney & blood pressure research</title><addtitle>Kidney Blood Press Res</addtitle><description>Background/Aims: The contribution of emergent cardiovascular risk factors to atherosclerotic renal artery stenosis (ARAS) is debated. We investigated the relationship of lipoprotein(a) and prothrombotic factors with ARAS in hypertension. Methods: In 50 hypertensive patients with angiographic evidence of ARAS and 58 hypertensive patients who had comparable cardiovascular risk factor burden but no evidence of renovascular disease, we measured renal function, lipoprotein(a), homocysteine, and hemostatic-fibrinolytic markers. Results: Patients with ARAS were more frequently smokers and had longer duration of hypertension, heavier antihypertensive treatment, and worse renal function than controls. Lipoprotein(a) was higher in patients with ARAS than controls, whereas no differences were found in homocysteine and all hemostatic variables. Multivariate analysis showed that lipoprotein(a) was associated with ARAS independent of other confounders including renal function and history of coronary heart, cerebrovascular, and peripheral artery disease. Conclusion: Lipoprotein(a) might contribute to the development of ARAS and detection of elevated levels of this lipoprotein could raise the suspicion of renovascular disease in patients with high blood pressure.</description><subject>Aged</subject><subject>Atherosclerosis - etiology</subject><subject>Atherosclerosis - pathology</subject><subject>Complications and side effects</subject><subject>Cross-Sectional Studies</subject><subject>Diagnosis</subject><subject>Female</subject><subject>Fibrinolysis</subject><subject>Health aspects</subject><subject>Hemostasis</subject><subject>Homocysteine</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - complications</subject><subject>Hypertension - pathology</subject><subject>Ischemic nephropathy</subject><subject>Kidney Function Tests</subject><subject>Lipoprotein A</subject><subject>Lipoprotein(a) - blood</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Prothrombotic state</subject><subject>Renal artery obstruction</subject><subject>Renal Artery Obstruction - etiology</subject><subject>Renal Artery Obstruction - pathology</subject><subject>Renovascular hypertension</subject><subject>Risk Factors</subject><issn>1420-4096</issn><issn>1423-0143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkU1v1DAQhiMEoqVw4I5QpF7aQ4o_ktg5LhX9ECtRFThbE2e8eEns1M5W2n-Ptyk5IDSSbY2fef16JsveU3JBadV8IoTwWpYNe5Ed05LxgtCSv3w6k6IkTX2UvYlxm7CKEPY6O2KVFJTz-jhTdz3EAfK1Hf0Y_ITWncF5vsZH7GMOrstX0y8MPuo-rZPV-T066PNVmDDs8-8TOh9tzK3Lb_YjpqyL9hHzO5gsuim-zV4Z6CO-e95Psp9XX35c3hTrb9e3l6t1oStOpkKjNNAhgbaUlYaWtbxpSFe1pJYSeF1rkLoGyRnSUrRIGkK6pm1aJiqOwvCT7HbW7Txs1RjsAGGvPFj1lPBhoyAk-z0q0zBmkh4pQZfMtLIy0ghtBG1pJalIWmezVmrIww7jpAYbNfY9OPS7qGgthJSypCyhp_-gW78LqUGJElwSKkh5oC5magPpfeuMnwLoFB0OVnuHxqb8quaCpWgODs7nAp06HwOa5UeUqMPI1TLyxH58trBrB-wW8u-ME_BhBn5D2GBYgKX-9L_XXz_fz4QaO8P_AB_tugw</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Catena, Cristiana</creator><creator>Colussi, GianLuca</creator><creator>Nait, Francesca</creator><creator>Capobianco, Frine</creator><creator>Sechi, Leonardo A</creator><general>S. 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Colussi, GianLuca ; Nait, Francesca ; Capobianco, Frine ; Sechi, Leonardo A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c530t-ce8fade0ab485cab2b3990d5b0688a366ca8c6a832e147be0900d9b9b2753e7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>Atherosclerosis - etiology</topic><topic>Atherosclerosis - pathology</topic><topic>Complications and side effects</topic><topic>Cross-Sectional Studies</topic><topic>Diagnosis</topic><topic>Female</topic><topic>Fibrinolysis</topic><topic>Health aspects</topic><topic>Hemostasis</topic><topic>Homocysteine</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - complications</topic><topic>Hypertension - pathology</topic><topic>Ischemic nephropathy</topic><topic>Kidney Function Tests</topic><topic>Lipoprotein A</topic><topic>Lipoprotein(a) - blood</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>Prothrombotic state</topic><topic>Renal artery obstruction</topic><topic>Renal Artery Obstruction - etiology</topic><topic>Renal Artery Obstruction - pathology</topic><topic>Renovascular hypertension</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Catena, Cristiana</creatorcontrib><creatorcontrib>Colussi, GianLuca</creatorcontrib><creatorcontrib>Nait, Francesca</creatorcontrib><creatorcontrib>Capobianco, Frine</creatorcontrib><creatorcontrib>Sechi, Leonardo A</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Kidney & blood pressure research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Catena, Cristiana</au><au>Colussi, GianLuca</au><au>Nait, Francesca</au><au>Capobianco, Frine</au><au>Sechi, Leonardo A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasma Lipoprotein(a) Levels and Atherosclerotic Renal Artery Stenosis in Hypertensive Patients</atitle><jtitle>Kidney & blood pressure research</jtitle><addtitle>Kidney Blood Press Res</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>40</volume><issue>2</issue><spage>166</spage><epage>175</epage><pages>166-175</pages><issn>1420-4096</issn><eissn>1423-0143</eissn><coden>RPBIEL</coden><abstract>Background/Aims: The contribution of emergent cardiovascular risk factors to atherosclerotic renal artery stenosis (ARAS) is debated. We investigated the relationship of lipoprotein(a) and prothrombotic factors with ARAS in hypertension. Methods: In 50 hypertensive patients with angiographic evidence of ARAS and 58 hypertensive patients who had comparable cardiovascular risk factor burden but no evidence of renovascular disease, we measured renal function, lipoprotein(a), homocysteine, and hemostatic-fibrinolytic markers. Results: Patients with ARAS were more frequently smokers and had longer duration of hypertension, heavier antihypertensive treatment, and worse renal function than controls. Lipoprotein(a) was higher in patients with ARAS than controls, whereas no differences were found in homocysteine and all hemostatic variables. Multivariate analysis showed that lipoprotein(a) was associated with ARAS independent of other confounders including renal function and history of coronary heart, cerebrovascular, and peripheral artery disease. Conclusion: Lipoprotein(a) might contribute to the development of ARAS and detection of elevated levels of this lipoprotein could raise the suspicion of renovascular disease in patients with high blood pressure.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>25871336</pmid><doi>10.1159/000368492</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Atherosclerosis - etiology Atherosclerosis - pathology Complications and side effects Cross-Sectional Studies Diagnosis Female Fibrinolysis Health aspects Hemostasis Homocysteine Humans Hypertension Hypertension - complications Hypertension - pathology Ischemic nephropathy Kidney Function Tests Lipoprotein A Lipoprotein(a) - blood Male Middle Aged Original Paper Prothrombotic state Renal artery obstruction Renal Artery Obstruction - etiology Renal Artery Obstruction - pathology Renovascular hypertension Risk Factors |
| title | Plasma Lipoprotein(a) Levels and Atherosclerotic Renal Artery Stenosis in Hypertensive Patients |
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