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Article: Associations of serum fetuin-A with malnutrition, inflammation, atherosclerosis and valvular calcification syndrome and outcome in peritoneal dialysis patients

TitleAssociations of serum fetuin-A with malnutrition, inflammation, atherosclerosis and valvular calcification syndrome and outcome in peritoneal dialysis patients
Authors
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/
Citation
Nephrology Dialysis Transplantation, 2005, v. 20 n. 8, p. 1676-1685 How to Cite?
AbstractBackground. Fetuin-A (α 2-Heremans Schmid glycoprotein) has recently been identified as a circulating inhibitor of calcification and is regulated as a negative acute phase protein. However, its relationships with cardiac valvular calcification and atherosclerosis and outcome have not been evaluated in peritoneal dialysis (PD) patients. Method. We performed a prospective follow-up study in 238 PD patients with echocardiography done at baseline to detect cardiac valvular calcification and biochemical analysis performed for serum fetuin-A, albumin and C-reactive protein (CRP). Results. Baseline serum fetuin-A concentration was (mean±SD) 0.309±0.068 g/l (normal range 0.4-0.95). Across the three tertiles of increasing serum fetuin-A, a significant trend effect was observed for age (P = 0.023), diabetes (P = 0.008), background atherosclerotic vascular disease (P = 0.010), cardiac valvular calcification (P = 0.002), serum albumin (P<0.001), subjective global assessment (P = 0.005) and CRP (P<0.001). Adjusti0ng for CRP and calcium × phosphorus product, every 0.01 g/l increase in serum fetuin-A remained independently associated with a 6% decrease in the risk of valvular calcification (95% confidence intervals, 0.90-0.99; P = 0.028). Furthermore, serum fetuin-A showed a significant decrease across the four groups of patients with increasing components of the malnutrition, inflammation, atherosclerosis/calcification (MIAC) syndrome (P<0.001) and was the lowest among patients with all components of the MIAC syndrome (0.263±0.055 g/l) and highest among those who do not have the MIAC syndrome at all (0.338±0.06 g/l). Lower serum fetuin-A was associated with greater all-cause mortality (P = 0.0011) and fatal and non-fatal cardiovascular events (P = 0.0017), but its significance was lost when atherosclerotic vascular disease, valvular calcification, inflammation and malnutrition were included in the model. Conclusions. Serum fetuin-A showed important associations with valvular calcification, atherosclerosis, malnutrition and inflammation, and was linked to mortality and cardiovascular events in PD patients via its close relationships with the MIAC syndrome. © The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/162888
ISSN
2015 Impact Factor: 4.085
2015 SCImago Journal Rankings: 1.780
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, AYMen_US
dc.contributor.authorWoo, Jen_US
dc.contributor.authorLam, CWKen_US
dc.contributor.authorWang, Men_US
dc.contributor.authorChan, IHSen_US
dc.contributor.authorGao, Pen_US
dc.contributor.authorLui, SFen_US
dc.contributor.authorLi, PKTen_US
dc.contributor.authorSanderson, JEen_US
dc.date.accessioned2012-09-05T05:24:50Z-
dc.date.available2012-09-05T05:24:50Z-
dc.date.issued2005en_US
dc.identifier.citationNephrology Dialysis Transplantation, 2005, v. 20 n. 8, p. 1676-1685en_US
dc.identifier.issn0931-0509en_US
dc.identifier.urihttp://hdl.handle.net/10722/162888-
dc.description.abstractBackground. Fetuin-A (α 2-Heremans Schmid glycoprotein) has recently been identified as a circulating inhibitor of calcification and is regulated as a negative acute phase protein. However, its relationships with cardiac valvular calcification and atherosclerosis and outcome have not been evaluated in peritoneal dialysis (PD) patients. Method. We performed a prospective follow-up study in 238 PD patients with echocardiography done at baseline to detect cardiac valvular calcification and biochemical analysis performed for serum fetuin-A, albumin and C-reactive protein (CRP). Results. Baseline serum fetuin-A concentration was (mean±SD) 0.309±0.068 g/l (normal range 0.4-0.95). Across the three tertiles of increasing serum fetuin-A, a significant trend effect was observed for age (P = 0.023), diabetes (P = 0.008), background atherosclerotic vascular disease (P = 0.010), cardiac valvular calcification (P = 0.002), serum albumin (P<0.001), subjective global assessment (P = 0.005) and CRP (P<0.001). Adjusti0ng for CRP and calcium × phosphorus product, every 0.01 g/l increase in serum fetuin-A remained independently associated with a 6% decrease in the risk of valvular calcification (95% confidence intervals, 0.90-0.99; P = 0.028). Furthermore, serum fetuin-A showed a significant decrease across the four groups of patients with increasing components of the malnutrition, inflammation, atherosclerosis/calcification (MIAC) syndrome (P<0.001) and was the lowest among patients with all components of the MIAC syndrome (0.263±0.055 g/l) and highest among those who do not have the MIAC syndrome at all (0.338±0.06 g/l). Lower serum fetuin-A was associated with greater all-cause mortality (P = 0.0011) and fatal and non-fatal cardiovascular events (P = 0.0017), but its significance was lost when atherosclerotic vascular disease, valvular calcification, inflammation and malnutrition were included in the model. Conclusions. Serum fetuin-A showed important associations with valvular calcification, atherosclerosis, malnutrition and inflammation, and was linked to mortality and cardiovascular events in PD patients via its close relationships with the MIAC syndrome. © The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/en_US
dc.relation.ispartofNephrology Dialysis Transplantationen_US
dc.subject.meshArteriosclerosis - Blood - Etiologyen_US
dc.subject.meshBlood Proteins - Metabolismen_US
dc.subject.meshC-Reactive Protein - Metabolismen_US
dc.subject.meshCalcinosis - Blood - Etiologyen_US
dc.subject.meshEchocardiographyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFollow-Up Studiesen_US
dc.subject.meshHeart Valve Diseases - Blood - Etiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInflammation - Blood - Etiologyen_US
dc.subject.meshKidney Failure, Chronic - Therapyen_US
dc.subject.meshMaleen_US
dc.subject.meshMalnutrition - Blooden_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPeritoneal Dialysisen_US
dc.subject.meshProspective Studiesen_US
dc.subject.meshSerum Albumin - Metabolismen_US
dc.subject.meshSurvival Rateen_US
dc.subject.meshSyndromeen_US
dc.subject.meshAlpha-2-Hs-Glycoproteinen_US
dc.titleAssociations of serum fetuin-A with malnutrition, inflammation, atherosclerosis and valvular calcification syndrome and outcome in peritoneal dialysis patientsen_US
dc.typeArticleen_US
dc.identifier.emailWang, M:meiwang@hkucc.hku.hken_US
dc.identifier.authorityWang, M=rp00281en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/ndt/gfh891en_US
dc.identifier.pmid15899935-
dc.identifier.scopuseid_2-s2.0-26444541329en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-26444541329&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume20en_US
dc.identifier.issue8en_US
dc.identifier.spage1676en_US
dc.identifier.epage1685en_US
dc.identifier.isiWOS:000231055400024-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridWang, AYM=13606226000en_US
dc.identifier.scopusauthoridWoo, J=36040369400en_US
dc.identifier.scopusauthoridLam, CWK=8531362100en_US
dc.identifier.scopusauthoridWang, M=7406690398en_US
dc.identifier.scopusauthoridChan, IHS=8298775100en_US
dc.identifier.scopusauthoridGao, P=55065678700en_US
dc.identifier.scopusauthoridLui, SF=7102379144en_US
dc.identifier.scopusauthoridLi, PKT=25928016800en_US
dc.identifier.scopusauthoridSanderson, JE=7202371250en_US
dc.identifier.citeulike264676-

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