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Article: Is valvular calcification a part of the missing link between residual kidney function and cardiac hypertrophy in peritoneal dialysis patients?

TitleIs valvular calcification a part of the missing link between residual kidney function and cardiac hypertrophy in peritoneal dialysis patients?
Authors
Issue Date2009
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.cjasn.org
Citation
Clinical Journal Of The American Society Of Nephrology, 2009, v. 4 n. 10, p. 1629-1636 How to Cite?
AbstractBackground and objectives: Residual renal function (RRF) predicts survival and shows an important inverse relation with cardiac hypertrophy in peritoneal dialysis (PD) patients. We hypothesized that valvular calcification and the calcification milieu may be part of the process linking loss of RRF and cardiac hypertrophy. Design, setting, participants, & measurements: A cross-sectional study was conducted by performing two-dimensional echocardiography on 230 PD patients to assess valvular calcification and left ventricular (LV) mass and collecting 24-h urine for estimation of RRF. Results: Patients having valvular calcification had lower RRF than those without. Patients with no RRF showed higher calcium-phosphorus product (Ca x P) and C-reactive protein (CRP). Using multiple logistic regression analysis, every 1-ml/min per 1.73 m 2 increase in residual GFR was associated with a 28% reduction in the risk for valvular calcification. The association was lost after additional adjustment for Ca x P and CRP. Using multiple linear regression analysis, loss of RRF showed significant association with increased LV mass index, but this association was lost after additional adjustment for CRP, Ca x P, and valvular calcification. Patients with all three calcification risk factors, namely inflammation, high Ca x P, and no RRF, showed the highest prevalence of valvular calcification and had the most severe cardiac hypertrophy. Conclusions: The association among loss of RRF, valvular calcification, and cardiac hypertrophy was closely linked to increased inflammation and high Ca x P in PD patients. These data suggest that valvular calcification and the calcification milieu are part of the processes linking loss of RRF and worsening cardiac hypertrophy in PD. Copyright © 2009 by the American Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/163287
ISSN
2015 Impact Factor: 4.657
2015 SCImago Journal Rankings: 2.534
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, AYMen_US
dc.contributor.authorLam, CWKen_US
dc.contributor.authorWang, Men_US
dc.contributor.authorChan, IHSen_US
dc.contributor.authorLui, SFen_US
dc.contributor.authorSanderson, JEen_US
dc.date.accessioned2012-09-05T05:29:39Z-
dc.date.available2012-09-05T05:29:39Z-
dc.date.issued2009en_US
dc.identifier.citationClinical Journal Of The American Society Of Nephrology, 2009, v. 4 n. 10, p. 1629-1636en_US
dc.identifier.issn1555-9041en_US
dc.identifier.urihttp://hdl.handle.net/10722/163287-
dc.description.abstractBackground and objectives: Residual renal function (RRF) predicts survival and shows an important inverse relation with cardiac hypertrophy in peritoneal dialysis (PD) patients. We hypothesized that valvular calcification and the calcification milieu may be part of the process linking loss of RRF and cardiac hypertrophy. Design, setting, participants, & measurements: A cross-sectional study was conducted by performing two-dimensional echocardiography on 230 PD patients to assess valvular calcification and left ventricular (LV) mass and collecting 24-h urine for estimation of RRF. Results: Patients having valvular calcification had lower RRF than those without. Patients with no RRF showed higher calcium-phosphorus product (Ca x P) and C-reactive protein (CRP). Using multiple logistic regression analysis, every 1-ml/min per 1.73 m 2 increase in residual GFR was associated with a 28% reduction in the risk for valvular calcification. The association was lost after additional adjustment for Ca x P and CRP. Using multiple linear regression analysis, loss of RRF showed significant association with increased LV mass index, but this association was lost after additional adjustment for CRP, Ca x P, and valvular calcification. Patients with all three calcification risk factors, namely inflammation, high Ca x P, and no RRF, showed the highest prevalence of valvular calcification and had the most severe cardiac hypertrophy. Conclusions: The association among loss of RRF, valvular calcification, and cardiac hypertrophy was closely linked to increased inflammation and high Ca x P in PD patients. These data suggest that valvular calcification and the calcification milieu are part of the processes linking loss of RRF and worsening cardiac hypertrophy in PD. Copyright © 2009 by the American Society of Nephrology.en_US
dc.languageengen_US
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at http://www.cjasn.orgen_US
dc.relation.ispartofClinical Journal of the American Society of Nephrologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshC-Reactive Protein - Analysisen_US
dc.subject.meshCalcinosis - Complicationsen_US
dc.subject.meshCross-Sectional Studiesen_US
dc.subject.meshEchocardiographyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGlomerular Filtration Rateen_US
dc.subject.meshHeart Valve Diseases - Complicationsen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertrophy, Left Ventricular - Etiologyen_US
dc.subject.meshLinear Modelsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPeritoneal Dialysis - Adverse Effectsen_US
dc.titleIs valvular calcification a part of the missing link between residual kidney function and cardiac hypertrophy in peritoneal dialysis patients?en_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.doi10.2215/CJN.03100509en_US
dc.identifier.pmid19713292-
dc.identifier.scopuseid_2-s2.0-73349126112en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-73349126112&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume4en_US
dc.identifier.issue10en_US
dc.identifier.spage1629en_US
dc.identifier.epage1636en_US
dc.identifier.isiWOS:000270617900014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, AYM=13606226000en_US
dc.identifier.scopusauthoridLam, CWK=8531362100en_US
dc.identifier.scopusauthoridWang, M=7406690398en_US
dc.identifier.scopusauthoridChan, IHS=8298775100en_US
dc.identifier.scopusauthoridLui, SF=7102379144en_US
dc.identifier.scopusauthoridSanderson, JE=7202371250en_US

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