{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T05:55:01Z","timestamp":1790488501587,"version":"4.1.0"},"reference-count":27,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2016,5,17]],"date-time":"2016-05-17T00:00:00Z","timestamp":1463443200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2016,6]]},"abstract":"Abstract<\/jats:title>\n \n Aim<\/jats:title>\n Patients with chronic heart failure (CHF) are often characterized by the cardiorenal syndrome (CRS). The aim of the present study was to assess whether novel markers of kidney injury are able to predict progression of chronic kidney disease (CKD) in patients with CHF.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n New renal biomarkers, N\u2010acteyl\u2010\u00df\u2010D\u2010glucosaminidase (NAG), kidney injury molecule\u20101 (KIM\u20101) and Neutrophil Gelatinase\u2010Associated Lipocalin (NGAL), were assessed from urine samples of 149 patients with chronic heart failure. During a 5\u2010year\u2010follow\u2010up, renal function was assessed by creatinine and estimated glomerular filtration rate (eGFR CKD EPI) and was available for 138 patients. Further, data regarding all\u2010cause mortality was obtained.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Twenty\u2010six patients (18.8%) developed a progression of CKD during the follow\u2010up period, as defined by decline in eGFR category accompanied by a \u226525% drop in eGFR form baseline. No difference regarding age, sex, body mass index, hypertension, diabetes or EF was present between patients with and without CKD progression (each\n P\u2009=<\/jats:italic>\n \u2009n.s.). At baseline, creatinine concentrations and eGFR were significantly different between both groups (sCr: 1.50 \u00b1 0.67 vs 1.04 \u00b1 0.37,\n P\u2009=<\/jats:italic>\n \u2009<\u20090.001; eGFR: 47.8 \u00b1 12.3 vs. 77.3 \u00b1 23.5 mL\/min per 1.73m\n 2<\/jats:sup>\n , each\n P\u2009<<\/jats:italic>\n \u20090.001). In a Kaplan\u2013Meier\u2010analysis, KIM\u20101 and NAG were significant predictors for CKD progression (both\n P\u2009<<\/jats:italic>\n \u20090.05). In Cox regression analysis, NAG > median (OR 3.25,\n P<\/jats:italic>\n \u2009=\u20090.013), initial eGFR (OR 0.94,\n P\u2009<<\/jats:italic>\n \u20090.001) and diuretic use (OR 3.92,\n P\u2009=<\/jats:italic>\n \u20090.001) were independent predictors of CKD progression. Further, KIM\u20101 and NAG were also independent predictors of a combined endpoint of CKD progression and all\u2010cause mortality by Cox regression analysis (each\n P\u2009<<\/jats:italic>\n \u20090.05). The combination of both markers showed additive value regarding both endpoints. NGAL showed no association with CKD progression.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n During long\u2010term follow\u2010up chronic heart failure patients with CKD show a relevant disease progression. The current study emphasizes a strong association of the tubular biomarkers NAG and KIM\u20101 with CKD progression in chronic heart failure and suggests their usefulness as cardiorenal markers.<\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/nep.12632","type":"journal-article","created":{"date-parts":[[2015,9,30]],"date-time":"2015-09-30T13:17:34Z","timestamp":1443619054000},"page":"490-498","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["N\u2010acteyl\u2010\u00df\u2010D\u2010glucosaminidase and kidney injury molecule\u20101: New predictors for long\u2010term progression of chronic kidney disease in patients with heart failure"],"prefix":"10.1111","volume":"21","author":[{"given":"Carsten G.","family":"Jungbauer","sequence":"first","affiliation":[{"name":"Department of Internal Medicine II University Hospital Regensburg Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ekrem","family":"Uecer","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II University Hospital Regensburg Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Stadler","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II University Hospital Regensburg Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christoph","family":"Birner","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II University Hospital Regensburg Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Buchner","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II University Hospital Regensburg Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars S.","family":"Maier","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II University Hospital Regensburg Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Luchner","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II University Hospital Regensburg Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,5,17]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2008.07.051"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0803"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardfail.2007.03.011"},{"key":"e_1_2_8_5_1","first-page":"351291","article-title":"Heart\u2010kidney interaction: epidemiology of cardiorenal syndromes","volume":"2011","author":"Cruz DN","year":"2010","journal-title":"Int J Nephrol"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000143547.55093.17"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1136\/hrt.2010.194878"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1093\/eurjhf\/hfr102"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.7.4135"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.3736\/jcim20080520"},{"issue":"1","key":"e_1_2_8_11_1","first-page":"14","article-title":"The role of NAG (N\u2010acetyl\u2010beta\u2010D\u2010glucosaminidase) in the diagnosis of kidney disease including the monitoring of nephrotoxicity","volume":"38","author":"Price RG","year":"1992","journal-title":"Clin. 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