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Proprotein convertase subtilisin–kexin type 9 is elevated in proteinuric subjects: Relationship with lipoprotein response to antiproteinuric treatment
Abstract Objective LDL-receptor deficiency may provide a mechanism which contributes to atherogenic lipoprotein abnormalities in experimental nephrosis and in humans with glomerular proteinuria. The proprotein convertase subtilisin–kexin type 9 (PCSK9) pathway plays a key role in lipoprotein metabol...
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| Published in: | Atherosclerosis 2013-02, Vol.226 (2), p.459-465 |
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| creator | Kwakernaak, Arjan J Lambert, Gilles Slagman, Maartje C.J Waanders, Femke Laverman, Gozewijn D Petrides, Francine Dikkeschei, Bert D Navis, Gerjan Dullaart, Robin P.F |
| description | Abstract Objective LDL-receptor deficiency may provide a mechanism which contributes to atherogenic lipoprotein abnormalities in experimental nephrosis and in humans with glomerular proteinuria. The proprotein convertase subtilisin–kexin type 9 (PCSK9) pathway plays a key role in lipoprotein metabolism by promoting LDL-receptor degradation. We tested whether plasma PCSK9 is elevated in proteinuric states, and determined relationships of PCSK9 with lipoprotein responses to proteinuria reduction. Methods Thirty-nine kidney patients (e-GFR 61 ± 29 mL/min/1.73 m2 , proteinuria 1.9 [0.9–3.3] g/day; 19 on statin treatment) were studied during 2 randomized double-blind 6-week periods on either lisinopril (40 mg/day) and a regular sodium diet (194 ± 49 mmol Na+/day; baseline treatment) or lisinopril plus valsartan (320 mg/day) and a low sodium diet (102 ± 52 mmol Na+ /day; maximal treatment), and compared to age- and sex-matched controls. Maximal treatment decreased proteinuria to 0.5 [0.3–1.1] g/day ( P |
| doi_str_mv | 10.1016/j.atherosclerosis.2012.11.009 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1273540408</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0021915012008040</els_id><sourcerecordid>1273540408</sourcerecordid><originalsourceid>FETCH-LOGICAL-c498t-9328a8ac9cc9ae558db110cb2a8d4f8617e14fd99d2b5e6805c160f5ad3b5f6a3</originalsourceid><addsrcrecordid>eNqNks9uEzEQxlcIREPhFcCXSlwSZrx_YiOBhCooSJVAlJ4tr3eWON14t7Y3kBvvwIXn40nwKiFCPXGxJc_vm_k0n7PsDGGBgNWL9ULHFfk-mG46bVhwQL5AXADIe9kMxVLOsRDF_WwGwHEusYST7FEIawAoligeZic85xXiks-yX598P_g-knXM9G5LPupALIx1tJ0N1v3-8fOGvqdq3A3EJLOBUUdbHalh6fWgHb01k2hNJoaX7DN1OtrehZUd2DcbV6yzw3GOpzCkGrHYM-2i_bdH9KTjhlx8nD1odRfoyeE-za7fvf1y_n5--fHiw_mby7kppIhzmXOhhTbSGKmpLEVTI4KpuRZN0YoKl4RF20jZ8LqkSkBpsIK21E1el22l89Ps-b5vcnE7UohqY4OhrtOO-jEo5Mu8LKAAkdBXe9SkxQdPrRq83Wi_UwhqCket1Z1w1BSOQlQpnKR_ehg11htqjuq_aSTg7ADoYHTXeu1M6nHkKpGDgIl7tuda3Sv91Sfm-ipNKqeEhayKRFzsCUqr21ryKhhLzlBjfYpINb39b9Ov73QynXU22buhHYV1P3qX8lGoAlegrqY_N3055JC8FpD_AfiA2_A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1273540408</pqid></control><display><type>article</type><title>Proprotein convertase subtilisin–kexin type 9 is elevated in proteinuric subjects: Relationship with lipoprotein response to antiproteinuric treatment</title><source>ScienceDirect Journals</source><creator>Kwakernaak, Arjan J ; Lambert, Gilles ; Slagman, Maartje C.J ; Waanders, Femke ; Laverman, Gozewijn D ; Petrides, Francine ; Dikkeschei, Bert D ; Navis, Gerjan ; Dullaart, Robin P.F</creator><creatorcontrib>Kwakernaak, Arjan J ; Lambert, Gilles ; Slagman, Maartje C.J ; Waanders, Femke ; Laverman, Gozewijn D ; Petrides, Francine ; Dikkeschei, Bert D ; Navis, Gerjan ; Dullaart, Robin P.F</creatorcontrib><description>Abstract Objective LDL-receptor deficiency may provide a mechanism which contributes to atherogenic lipoprotein abnormalities in experimental nephrosis and in humans with glomerular proteinuria. The proprotein convertase subtilisin–kexin type 9 (PCSK9) pathway plays a key role in lipoprotein metabolism by promoting LDL-receptor degradation. We tested whether plasma PCSK9 is elevated in proteinuric states, and determined relationships of PCSK9 with lipoprotein responses to proteinuria reduction. Methods Thirty-nine kidney patients (e-GFR 61 ± 29 mL/min/1.73 m2 , proteinuria 1.9 [0.9–3.3] g/day; 19 on statin treatment) were studied during 2 randomized double-blind 6-week periods on either lisinopril (40 mg/day) and a regular sodium diet (194 ± 49 mmol Na+/day; baseline treatment) or lisinopril plus valsartan (320 mg/day) and a low sodium diet (102 ± 52 mmol Na+ /day; maximal treatment), and compared to age- and sex-matched controls. Maximal treatment decreased proteinuria to 0.5 [0.3–1.1] g/day ( P < 0.001). Results Plasma PCSK9 was increased at baseline in proteinuric subjects (213 [161–314] vs. 143 [113–190] ug/L in controls, P ≤ 0.001), irrespective of statin use, e-GFR and BMI. PCSK9 correlated with proteinuria at baseline ( R = 0.399, P = 0.018) and at maximal antiproteinuric treatment ( R = 0.525, P = 0.001), but did not decrease during proteinuria reduction ( P = 0.84). Individual changes in total cholesterol ( R = 0.365, P = 0.024), non-HDL cholesterol ( R = 0.333, P = 0.041), and LDL cholesterol ( R = 0.346, P = 0.033) were correlated positively with individual PCSK9 responses. PCSK9 at baseline independently predicted the total/HDL cholesterol ratio response to treatment ( P = 0.04). Conclusion Plasma PCSK9 was elevated in proteinuria, predicted lipoprotein responses to proteinuria reduction but remained unchanged after proteinuria reduction. Inhibition of the PCSK9 pathway may provide a novel treatment strategy in proteinuric subjects.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2012.11.009</identifier><identifier>PMID: 23261172</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>Adult ; Antiproteinuric treatment ; atherosclerosis ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; body mass index ; Cardiology. Vascular system ; Cardiovascular ; Chronic kidney disease ; correlation ; Diet, Sodium-Restricted ; Female ; General and cellular metabolism. Vitamins ; high density lipoprotein cholesterol ; Humans ; kidneys ; LDL cholesterol ; Lipoproteins - blood ; Lipoproteins - drug effects ; Lisinopril - therapeutic use ; low density lipoprotein cholesterol ; low sodium diet ; Male ; Medical sciences ; metabolism ; Middle Aged ; nephrosis ; Non-HDL cholesterol ; patients ; Pharmacology. Drug treatments ; Proprotein Convertase 9 ; Proprotein convertase subtilisin–kexin type 9 ; Proprotein Convertases - blood ; Proteinuria ; Proteinuria - blood ; Proteinuria - drug therapy ; Proteinuria - enzymology ; Serine Endopeptidases - blood ; sodium ; Tetrazoles - therapeutic use ; Valine - analogs & derivatives ; Valine - therapeutic use ; Valsartan</subject><ispartof>Atherosclerosis, 2013-02, Vol.226 (2), p.459-465</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2012 Elsevier Ireland Ltd</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c498t-9328a8ac9cc9ae558db110cb2a8d4f8617e14fd99d2b5e6805c160f5ad3b5f6a3</citedby><cites>FETCH-LOGICAL-c498t-9328a8ac9cc9ae558db110cb2a8d4f8617e14fd99d2b5e6805c160f5ad3b5f6a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26830802$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23261172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kwakernaak, Arjan J</creatorcontrib><creatorcontrib>Lambert, Gilles</creatorcontrib><creatorcontrib>Slagman, Maartje C.J</creatorcontrib><creatorcontrib>Waanders, Femke</creatorcontrib><creatorcontrib>Laverman, Gozewijn D</creatorcontrib><creatorcontrib>Petrides, Francine</creatorcontrib><creatorcontrib>Dikkeschei, Bert D</creatorcontrib><creatorcontrib>Navis, Gerjan</creatorcontrib><creatorcontrib>Dullaart, Robin P.F</creatorcontrib><title>Proprotein convertase subtilisin–kexin type 9 is elevated in proteinuric subjects: Relationship with lipoprotein response to antiproteinuric treatment</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Abstract Objective LDL-receptor deficiency may provide a mechanism which contributes to atherogenic lipoprotein abnormalities in experimental nephrosis and in humans with glomerular proteinuria. The proprotein convertase subtilisin–kexin type 9 (PCSK9) pathway plays a key role in lipoprotein metabolism by promoting LDL-receptor degradation. We tested whether plasma PCSK9 is elevated in proteinuric states, and determined relationships of PCSK9 with lipoprotein responses to proteinuria reduction. Methods Thirty-nine kidney patients (e-GFR 61 ± 29 mL/min/1.73 m2 , proteinuria 1.9 [0.9–3.3] g/day; 19 on statin treatment) were studied during 2 randomized double-blind 6-week periods on either lisinopril (40 mg/day) and a regular sodium diet (194 ± 49 mmol Na+/day; baseline treatment) or lisinopril plus valsartan (320 mg/day) and a low sodium diet (102 ± 52 mmol Na+ /day; maximal treatment), and compared to age- and sex-matched controls. Maximal treatment decreased proteinuria to 0.5 [0.3–1.1] g/day ( P < 0.001). Results Plasma PCSK9 was increased at baseline in proteinuric subjects (213 [161–314] vs. 143 [113–190] ug/L in controls, P ≤ 0.001), irrespective of statin use, e-GFR and BMI. PCSK9 correlated with proteinuria at baseline ( R = 0.399, P = 0.018) and at maximal antiproteinuric treatment ( R = 0.525, P = 0.001), but did not decrease during proteinuria reduction ( P = 0.84). Individual changes in total cholesterol ( R = 0.365, P = 0.024), non-HDL cholesterol ( R = 0.333, P = 0.041), and LDL cholesterol ( R = 0.346, P = 0.033) were correlated positively with individual PCSK9 responses. PCSK9 at baseline independently predicted the total/HDL cholesterol ratio response to treatment ( P = 0.04). Conclusion Plasma PCSK9 was elevated in proteinuria, predicted lipoprotein responses to proteinuria reduction but remained unchanged after proteinuria reduction. Inhibition of the PCSK9 pathway may provide a novel treatment strategy in proteinuric subjects.</description><subject>Adult</subject><subject>Antiproteinuric treatment</subject><subject>atherosclerosis</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>body mass index</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Chronic kidney disease</subject><subject>correlation</subject><subject>Diet, Sodium-Restricted</subject><subject>Female</subject><subject>General and cellular metabolism. Vitamins</subject><subject>high density lipoprotein cholesterol</subject><subject>Humans</subject><subject>kidneys</subject><subject>LDL cholesterol</subject><subject>Lipoproteins - blood</subject><subject>Lipoproteins - drug effects</subject><subject>Lisinopril - therapeutic use</subject><subject>low density lipoprotein cholesterol</subject><subject>low sodium diet</subject><subject>Male</subject><subject>Medical sciences</subject><subject>metabolism</subject><subject>Middle Aged</subject><subject>nephrosis</subject><subject>Non-HDL cholesterol</subject><subject>patients</subject><subject>Pharmacology. Drug treatments</subject><subject>Proprotein Convertase 9</subject><subject>Proprotein convertase subtilisin–kexin type 9</subject><subject>Proprotein Convertases - blood</subject><subject>Proteinuria</subject><subject>Proteinuria - blood</subject><subject>Proteinuria - drug therapy</subject><subject>Proteinuria - enzymology</subject><subject>Serine Endopeptidases - blood</subject><subject>sodium</subject><subject>Tetrazoles - therapeutic use</subject><subject>Valine - analogs & derivatives</subject><subject>Valine - therapeutic use</subject><subject>Valsartan</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqNks9uEzEQxlcIREPhFcCXSlwSZrx_YiOBhCooSJVAlJ4tr3eWON14t7Y3kBvvwIXn40nwKiFCPXGxJc_vm_k0n7PsDGGBgNWL9ULHFfk-mG46bVhwQL5AXADIe9kMxVLOsRDF_WwGwHEusYST7FEIawAoligeZic85xXiks-yX598P_g-knXM9G5LPupALIx1tJ0N1v3-8fOGvqdq3A3EJLOBUUdbHalh6fWgHb01k2hNJoaX7DN1OtrehZUd2DcbV6yzw3GOpzCkGrHYM-2i_bdH9KTjhlx8nD1odRfoyeE-za7fvf1y_n5--fHiw_mby7kppIhzmXOhhTbSGKmpLEVTI4KpuRZN0YoKl4RF20jZ8LqkSkBpsIK21E1el22l89Ps-b5vcnE7UohqY4OhrtOO-jEo5Mu8LKAAkdBXe9SkxQdPrRq83Wi_UwhqCket1Z1w1BSOQlQpnKR_ehg11htqjuq_aSTg7ADoYHTXeu1M6nHkKpGDgIl7tuda3Sv91Sfm-ipNKqeEhayKRFzsCUqr21ryKhhLzlBjfYpINb39b9Ov73QynXU22buhHYV1P3qX8lGoAlegrqY_N3055JC8FpD_AfiA2_A</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>Kwakernaak, Arjan J</creator><creator>Lambert, Gilles</creator><creator>Slagman, Maartje C.J</creator><creator>Waanders, Femke</creator><creator>Laverman, Gozewijn D</creator><creator>Petrides, Francine</creator><creator>Dikkeschei, Bert D</creator><creator>Navis, Gerjan</creator><creator>Dullaart, Robin P.F</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>FBQ</scope><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20130201</creationdate><title>Proprotein convertase subtilisin–kexin type 9 is elevated in proteinuric subjects: Relationship with lipoprotein response to antiproteinuric treatment</title><author>Kwakernaak, Arjan J ; Lambert, Gilles ; Slagman, Maartje C.J ; Waanders, Femke ; Laverman, Gozewijn D ; Petrides, Francine ; Dikkeschei, Bert D ; Navis, Gerjan ; Dullaart, Robin P.F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-9328a8ac9cc9ae558db110cb2a8d4f8617e14fd99d2b5e6805c160f5ad3b5f6a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Antiproteinuric treatment</topic><topic>atherosclerosis</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>body mass index</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular</topic><topic>Chronic kidney disease</topic><topic>correlation</topic><topic>Diet, Sodium-Restricted</topic><topic>Female</topic><topic>General and cellular metabolism. Vitamins</topic><topic>high density lipoprotein cholesterol</topic><topic>Humans</topic><topic>kidneys</topic><topic>LDL cholesterol</topic><topic>Lipoproteins - blood</topic><topic>Lipoproteins - drug effects</topic><topic>Lisinopril - therapeutic use</topic><topic>low density lipoprotein cholesterol</topic><topic>low sodium diet</topic><topic>Male</topic><topic>Medical sciences</topic><topic>metabolism</topic><topic>Middle Aged</topic><topic>nephrosis</topic><topic>Non-HDL cholesterol</topic><topic>patients</topic><topic>Pharmacology. Drug treatments</topic><topic>Proprotein Convertase 9</topic><topic>Proprotein convertase subtilisin–kexin type 9</topic><topic>Proprotein Convertases - blood</topic><topic>Proteinuria</topic><topic>Proteinuria - blood</topic><topic>Proteinuria - drug therapy</topic><topic>Proteinuria - enzymology</topic><topic>Serine Endopeptidases - blood</topic><topic>sodium</topic><topic>Tetrazoles - therapeutic use</topic><topic>Valine - analogs & derivatives</topic><topic>Valine - therapeutic use</topic><topic>Valsartan</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kwakernaak, Arjan J</creatorcontrib><creatorcontrib>Lambert, Gilles</creatorcontrib><creatorcontrib>Slagman, Maartje C.J</creatorcontrib><creatorcontrib>Waanders, Femke</creatorcontrib><creatorcontrib>Laverman, Gozewijn D</creatorcontrib><creatorcontrib>Petrides, Francine</creatorcontrib><creatorcontrib>Dikkeschei, Bert D</creatorcontrib><creatorcontrib>Navis, Gerjan</creatorcontrib><creatorcontrib>Dullaart, Robin P.F</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kwakernaak, Arjan J</au><au>Lambert, Gilles</au><au>Slagman, Maartje C.J</au><au>Waanders, Femke</au><au>Laverman, Gozewijn D</au><au>Petrides, Francine</au><au>Dikkeschei, Bert D</au><au>Navis, Gerjan</au><au>Dullaart, Robin P.F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proprotein convertase subtilisin–kexin type 9 is elevated in proteinuric subjects: Relationship with lipoprotein response to antiproteinuric treatment</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>226</volume><issue>2</issue><spage>459</spage><epage>465</epage><pages>459-465</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Abstract Objective LDL-receptor deficiency may provide a mechanism which contributes to atherogenic lipoprotein abnormalities in experimental nephrosis and in humans with glomerular proteinuria. The proprotein convertase subtilisin–kexin type 9 (PCSK9) pathway plays a key role in lipoprotein metabolism by promoting LDL-receptor degradation. We tested whether plasma PCSK9 is elevated in proteinuric states, and determined relationships of PCSK9 with lipoprotein responses to proteinuria reduction. Methods Thirty-nine kidney patients (e-GFR 61 ± 29 mL/min/1.73 m2 , proteinuria 1.9 [0.9–3.3] g/day; 19 on statin treatment) were studied during 2 randomized double-blind 6-week periods on either lisinopril (40 mg/day) and a regular sodium diet (194 ± 49 mmol Na+/day; baseline treatment) or lisinopril plus valsartan (320 mg/day) and a low sodium diet (102 ± 52 mmol Na+ /day; maximal treatment), and compared to age- and sex-matched controls. Maximal treatment decreased proteinuria to 0.5 [0.3–1.1] g/day ( P < 0.001). Results Plasma PCSK9 was increased at baseline in proteinuric subjects (213 [161–314] vs. 143 [113–190] ug/L in controls, P ≤ 0.001), irrespective of statin use, e-GFR and BMI. PCSK9 correlated with proteinuria at baseline ( R = 0.399, P = 0.018) and at maximal antiproteinuric treatment ( R = 0.525, P = 0.001), but did not decrease during proteinuria reduction ( P = 0.84). Individual changes in total cholesterol ( R = 0.365, P = 0.024), non-HDL cholesterol ( R = 0.333, P = 0.041), and LDL cholesterol ( R = 0.346, P = 0.033) were correlated positively with individual PCSK9 responses. PCSK9 at baseline independently predicted the total/HDL cholesterol ratio response to treatment ( P = 0.04). Conclusion Plasma PCSK9 was elevated in proteinuria, predicted lipoprotein responses to proteinuria reduction but remained unchanged after proteinuria reduction. Inhibition of the PCSK9 pathway may provide a novel treatment strategy in proteinuric subjects.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>23261172</pmid><doi>10.1016/j.atherosclerosis.2012.11.009</doi><tpages>7</tpages></addata></record> |
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| ispartof | Atherosclerosis, 2013-02, Vol.226 (2), p.459-465 |
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| subjects | Adult Antiproteinuric treatment atherosclerosis Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels body mass index Cardiology. Vascular system Cardiovascular Chronic kidney disease correlation Diet, Sodium-Restricted Female General and cellular metabolism. Vitamins high density lipoprotein cholesterol Humans kidneys LDL cholesterol Lipoproteins - blood Lipoproteins - drug effects Lisinopril - therapeutic use low density lipoprotein cholesterol low sodium diet Male Medical sciences metabolism Middle Aged nephrosis Non-HDL cholesterol patients Pharmacology. Drug treatments Proprotein Convertase 9 Proprotein convertase subtilisin–kexin type 9 Proprotein Convertases - blood Proteinuria Proteinuria - blood Proteinuria - drug therapy Proteinuria - enzymology Serine Endopeptidases - blood sodium Tetrazoles - therapeutic use Valine - analogs & derivatives Valine - therapeutic use Valsartan |
| title | Proprotein convertase subtilisin–kexin type 9 is elevated in proteinuric subjects: Relationship with lipoprotein response to antiproteinuric treatment |
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