{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T02:17:52Z","timestamp":1790734672023,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","license":[{"start":{"date-parts":[[2018,10,8]],"date-time":"2018-10-08T00:00:00Z","timestamp":1538956800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004690","name":"Minist\u00e8re de la Sant\u00e9","doi-asserted-by":"publisher","award":["PHRC-UF 9763"],"award-info":[{"award-number":["PHRC-UF 9763"]}],"id":[{"id":"10.13039\/501100004690","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2018,10,8]]},"abstract":"Heart failure is the most frequent cardiac complication of chronic kidney disease (CKD). Biomarkers help identify high-risk patients. Natriuretic peptides (BNP and NT-proBNP) are largely used for monitoring patients with cardiac failure but are highly dependent on glomerular filtration rate (GFR). Soluble suppression of tumorigenicity 2 (sST2) biomarker is well identified in risk stratification of cardiovascular (CV) events in heart failure. Furthermore, sST2 is included in a bioclinical score to stratify mortality risk. The aims of this study were to evaluate (i) the interest of circulating sST2 level in heart dysfunction and (ii) the bioclinical score (Barcelona Bio-Heart Failure risk calculator) to predict the risk of composite outcome (major adverse coronary events) and mortality in the CKD population. A retrospective study was carried out on 218 CKD patients enrolled from 2004 to 2015 at Montpellier University Hospital. sST2 was measured by ELISA (Presage ST2\u00ae kit). GFR was estimated by the CKD-EPI equation (eGFR). Indices of cardiac parameters were performed by cardiac echography. No patient had reduced ejection fraction. 112 patients had left ventricular hypertrophy, and 184 presented cardiac dysfunction, with structural, functional abnormalities or both. sST2 was independent of age and eGFR (\u03c1<\/mml:mi>=<\/mml:mo>0.05<\/mml:mn><\/mml:math>, p<\/mml:mi>=<\/mml:mo>0.44<\/mml:mn><\/mml:math>, and \u03c1<\/mml:mi>=<\/mml:mo>\u2212<\/mml:mo>0.07<\/mml:mn><\/mml:math>, p<\/mml:mi>=<\/mml:mo>0.3<\/mml:mn><\/mml:math>, respectively). Regarding echocardiogram data, sST2 was correlated with left ventricular mass index (\u03c1<\/mml:mi>=<\/mml:mo>0.16<\/mml:mn><\/mml:math>, p<\/mml:mi>=<\/mml:mo>0.02<\/mml:mn><\/mml:math>), left atrial diameter (\u03c1<\/mml:mi>=<\/mml:mo>0.14<\/mml:mn><\/mml:math>, p<\/mml:mi>=<\/mml:mo>0.04<\/mml:mn><\/mml:math>), and volume index (\u03c1<\/mml:mi>=<\/mml:mo>0.13<\/mml:mn><\/mml:math>, p<\/mml:mi>=<\/mml:mo>0.05<\/mml:mn><\/mml:math>). sST2 alone did not change risk prediction of death and\/or CV events compared to natriuretic peptides. Included in the Barcelona Bio-Heart Failure (BCN Bio-HF) score, sST2 added value and better stratified the risk of CV events and\/or death in CKD patients (p<\/mml:mi><<\/mml:mo>0.0001<\/mml:mn><\/mml:math>). To conclude, sST2 was associated with cardiac remodeling independently of eGFR, unlike other cardiac biomarkers. Added to the BCN Bio-HF score, the risk stratification of death and\/or CV events in nondialyzed CKD patients was highly improved.<\/jats:p>","DOI":"10.1155\/2018\/3952526","type":"journal-article","created":{"date-parts":[[2018,10,8]],"date-time":"2018-10-08T19:38:15Z","timestamp":1539027495000},"page":"1-9","source":"Crossref","is-referenced-by-count":33,"title":["sST2 as a New Biomarker of Chronic Kidney Disease-Induced Cardiac Remodeling: Impact on Risk Prediction"],"prefix":"10.1155","volume":"2018","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6930-9426","authenticated-orcid":true,"given":"Ma\u00eblle","family":"Plawecki","sequence":"first","affiliation":[{"name":"D\u00e9partement de Biochimie-Hormonologie, CHU Montpellier, Universit\u00e9 de Montpellier, Montpellier, France"},{"name":"PhyMedExp, Universit\u00e9 de Montpellier, CNRS, INSERM, Montpellier, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marion","family":"Morena","sequence":"additional","affiliation":[{"name":"D\u00e9partement de Biochimie-Hormonologie, CHU Montpellier, Universit\u00e9 de Montpellier, Montpellier, France"},{"name":"PhyMedExp, Universit\u00e9 de Montpellier, CNRS, INSERM, Montpellier, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nils","family":"Kuster","sequence":"additional","affiliation":[{"name":"D\u00e9partement de Biochimie-Hormonologie, CHU Montpellier, Universit\u00e9 de Montpellier, Montpellier, France"},{"name":"PhyMedExp, Universit\u00e9 de Montpellier, CNRS, INSERM, Montpellier, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leila","family":"Chenine","sequence":"additional","affiliation":[{"name":"D\u00e9partement de N\u00e9phrologie, CHU Montpellier, Universit\u00e9 de Montpellier, Montpellier, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H\u00e9l\u00e8ne","family":"Leray-Moragues","sequence":"additional","affiliation":[{"name":"D\u00e9partement de N\u00e9phrologie, CHU Montpellier, Universit\u00e9 de Montpellier, Montpellier, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5826-5755","authenticated-orcid":true,"given":"Bernard","family":"Jover","sequence":"additional","affiliation":[{"name":"PhyMedExp, Universit\u00e9 de Montpellier, CNRS, INSERM, Montpellier, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre","family":"Fesler","sequence":"additional","affiliation":[{"name":"PhyMedExp, Universit\u00e9 de Montpellier, CNRS, INSERM, Montpellier, France"},{"name":"D\u00e9partement de M\u00e9decine Interne et Hypertension, CHU Montpellier, Universit\u00e9 de Montpellier, Montpellier, 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