Proprotein convertase subtilisin-kexin type 9 is elevated in proteinuric subjects: Relationship with lipoprotein response to antiproteinuric treatment
Identifieur interne : 004D24 ( Main/Exploration ); précédent : 004D23; suivant : 004D25Proprotein convertase subtilisin-kexin type 9 is elevated in proteinuric subjects: Relationship with lipoprotein response to antiproteinuric treatment
Auteurs : Arjan J. Kwakernaak [Pays-Bas] ; Gilles Lambert [Australie, France] ; Maartje C. J. Slagman [Pays-Bas] ; Femke Waanders [Pays-Bas] ; Gozewijn D. Laverman [Pays-Bas] ; Francine Petrides [Australie] ; Bert D. Dikkeschei [Pays-Bas] ; Gerjan Navis [Pays-Bas] ; Robin P. F. Dullaart [Pays-Bas]Source :
- Atherosclerosis [ 0021-9150 ] ; 2013.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
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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.
Affiliations:
- Australie, France, Pays-Bas
- Groningue (province), Nouvelle-Galles du Sud, Pays de la Loire
- Groningue (ville), Nantes, Sydney
- Université de Groningue, Université de Nantes
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Kwakernaak</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen</s1><s3>NLD</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Pays-Bas</country><wicri:noRegion>Department of Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen</wicri:noRegion><orgName type="university">Université de Groningue</orgName><placeName><settlement type="city">Groningue (ville)</settlement><region>Groningue (province)</region></placeName></affiliation></author><author><name sortKey="Lambert, Gilles" sort="Lambert, Gilles" uniqKey="Lambert G" first="Gilles" last="Lambert">Gilles Lambert</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>The Heart Research Institute</s1><s2>Sydney</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region></placeName></affiliation><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>Inserm U957, Université de Nantes, Faculté de Médecine</s1><s2>Nantes</s2><s3>FRA</s3><sZ>2 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Pays de la Loire</region><region type="old region">Pays de la Loire</region><settlement type="city">Nantes</settlement><settlement type="city">Nantes</settlement></placeName><orgName type="university">Université de Nantes</orgName></affiliation></author><author><name sortKey="Slagman, Maartje C J" sort="Slagman, Maartje C J" uniqKey="Slagman M" first="Maartje C. J." last="Slagman">Maartje C. J. Slagman</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen</s1><s3>NLD</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Pays-Bas</country><wicri:noRegion>Department of Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen</wicri:noRegion><orgName type="university">Université de Groningue</orgName><placeName><settlement type="city">Groningue (ville)</settlement><region>Groningue (province)</region></placeName></affiliation></author><author><name sortKey="Waanders, Femke" sort="Waanders, Femke" uniqKey="Waanders F" first="Femke" last="Waanders">Femke Waanders</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen</s1><s3>NLD</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Pays-Bas</country><wicri:noRegion>Department of Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen</wicri:noRegion><orgName type="university">Université de Groningue</orgName><placeName><settlement type="city">Groningue (ville)</settlement><region>Groningue (province)</region></placeName></affiliation></author><author><name sortKey="Laverman, Gozewijn D" sort="Laverman, Gozewijn D" uniqKey="Laverman G" first="Gozewijn D." last="Laverman">Gozewijn D. Laverman</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Medicine, Division of Nephrology, ZGT Hospital</s1><s2>Almelo</s2><s3>NLD</s3><sZ>5 aut.</sZ></inist:fA14><country>Pays-Bas</country><wicri:noRegion>Almelo</wicri:noRegion></affiliation></author><author><name sortKey="Petrides, Francine" sort="Petrides, Francine" uniqKey="Petrides F" first="Francine" last="Petrides">Francine Petrides</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>The Heart Research Institute</s1><s2>Sydney</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region></placeName></affiliation></author><author><name sortKey="Dikkeschei, Bert D" sort="Dikkeschei, Bert D" uniqKey="Dikkeschei B" first="Bert D." last="Dikkeschei">Bert D. Dikkeschei</name><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Department of Clinical Chemistry, Isala Clinics</s1><s2>Zwolle</s2><s3>NLD</s3><sZ>7 aut.</sZ></inist:fA14><country>Pays-Bas</country><wicri:noRegion>Zwolle</wicri:noRegion></affiliation></author><author><name sortKey="Navis, Gerjan" sort="Navis, Gerjan" uniqKey="Navis G" first="Gerjan" last="Navis">Gerjan Navis</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen</s1><s3>NLD</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Pays-Bas</country><wicri:noRegion>Department of Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen</wicri:noRegion><orgName type="university">Université de Groningue</orgName><placeName><settlement type="city">Groningue (ville)</settlement><region>Groningue (province)</region></placeName></affiliation></author><author><name sortKey="Dullaart, Robin P F" sort="Dullaart, Robin P F" uniqKey="Dullaart R" first="Robin P. F." last="Dullaart">Robin P. F. Dullaart</name><affiliation wicri:level="4"><inist:fA14 i1="06"><s1>Department of Medicine, Division of Endocrinology, University of Groningen, University Medical Center Groningen</s1><s3>NLD</s3><sZ>9 aut.</sZ></inist:fA14><country>Pays-Bas</country><wicri:noRegion>Department of Medicine, Division of Endocrinology, University of Groningen, University Medical Center Groningen</wicri:noRegion><orgName type="university">Université de Groningue</orgName><placeName><settlement type="city">Groningue (ville)</settlement><region>Groningue (province)</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Atherosclerosis</title><title level="j" type="abbreviated">Atherosclerosis</title><idno type="ISSN">0021-9150</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Atherosclerosis</title><title level="j" type="abbreviated">Atherosclerosis</title><idno type="ISSN">0021-9150</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atherosclerosis</term><term>Cardiovascular disease</term><term>Cholesterol HDL</term><term>Cholesterol LDL</term><term>Chronic kidney disease</term><term>Human</term><term>Lipoprotein</term><term>Proteinuria</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Protéinurie</term><term>Néphropathie chronique</term><term>Pathologie de l'appareil circulatoire</term><term>Athérosclérose</term><term>Homme</term><term>Lipoprotéine</term><term>Traitement</term><term>Cholestérol LDL</term><term>Cholestérol HDL</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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 m<sup>2</sup>, 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<sup>+</sup>/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.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li><li>Pays-Bas</li></country><region><li>Groningue (province)</li><li>Nouvelle-Galles du Sud</li><li>Pays de la Loire</li></region><settlement><li>Groningue (ville)</li><li>Nantes</li><li>Sydney</li></settlement><orgName><li>Université de Groningue</li><li>Université de Nantes</li></orgName></list><tree><country name="Pays-Bas"><region name="Groningue (province)"><name sortKey="Kwakernaak, Arjan J" sort="Kwakernaak, Arjan J" uniqKey="Kwakernaak A" first="Arjan J." last="Kwakernaak">Arjan J. Kwakernaak</name></region><name sortKey="Dikkeschei, Bert D" sort="Dikkeschei, Bert D" uniqKey="Dikkeschei B" first="Bert D." last="Dikkeschei">Bert D. Dikkeschei</name><name sortKey="Dullaart, Robin P F" sort="Dullaart, Robin P F" uniqKey="Dullaart R" first="Robin P. F." last="Dullaart">Robin P. F. Dullaart</name><name sortKey="Laverman, Gozewijn D" sort="Laverman, Gozewijn D" uniqKey="Laverman G" first="Gozewijn D." last="Laverman">Gozewijn D. Laverman</name><name sortKey="Navis, Gerjan" sort="Navis, Gerjan" uniqKey="Navis G" first="Gerjan" last="Navis">Gerjan Navis</name><name sortKey="Slagman, Maartje C J" sort="Slagman, Maartje C J" uniqKey="Slagman M" first="Maartje C. J." last="Slagman">Maartje C. J. Slagman</name><name sortKey="Waanders, Femke" sort="Waanders, Femke" uniqKey="Waanders F" first="Femke" last="Waanders">Femke Waanders</name></country><country name="Australie"><region name="Nouvelle-Galles du Sud"><name sortKey="Lambert, Gilles" sort="Lambert, Gilles" uniqKey="Lambert G" first="Gilles" last="Lambert">Gilles Lambert</name></region><name sortKey="Petrides, Francine" sort="Petrides, Francine" uniqKey="Petrides F" first="Francine" last="Petrides">Francine Petrides</name></country><country name="France"><region name="Pays de la Loire"><name sortKey="Lambert, Gilles" sort="Lambert, Gilles" uniqKey="Lambert G" first="Gilles" last="Lambert">Gilles Lambert</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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