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Fibroblast growth factor 23 and matrix-metalloproteinases in patients with chronic kidney disease: are they associated with cardiovascular disease?

M. Peiskerová, M. Kalousová, M. Kratochvílová, S. Dusilová-Sulková, J. Uhrová, Š. Bandúr, I.M. Malbohan, T. Zima, V. Tesař

. 2009 ; 32 (4) : 276-283.

Language English Country Switzerland

Document type Research Support, Non-U.S. Gov't

Grant support
NS10043 MZ0 CEP Register

Digital library NLK
Full text - Article
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NLK Karger Journals from 1996 to 2009
ProQuest Central from 1994-05-01 to 1 year ago
Medline Complete (EBSCOhost) from 2005-01-01
Health & Medicine (ProQuest) from 1994-05-01 to 1 year ago
ROAD: Directory of Open Access Scholarly Resources from 1996

BACKGROUND: High cardiovascular risk in patients with chronic kidney disease (CKD) may be related to mineral disorder and microinflammation. Fibroblast growth factor 23 (FGF-23) is a phosphatonin and inhibitor of calcitriol synthesis, which is associated with poor prognosis in CKD patients starting dialysis. Matrix-metalloproteinases (MMP-2, MMP-9) contribute to myocardial remodeling and arterial calcification. FGF-23 and MMPs levels are altered in CKD, however, little is known about their association and relation to cardiovascular (CV) disease. METHODS: Standard laboratory parameters, plasma levels of MMP-2, MMP-9, FGF-23, PAPP-A and CV disease history were assessed in 80 patients with CKD 1-5 and 44 healthy control subjects. RESULTS: FGF-23 and MMP-2 (assessed by ELISA) were higher in CKD patients compared to controls. FGF-23 increased from CKD 3, whereas MMP-2 increased only in CKD 5. FGF-23 was positively associated with MMP-2, adjusted to age, eGFR, phosphatemia, calcitriol and parathormone. FGF-23 independently correlated with parathormone and inversely with calcitriol, whereas MMP-2 was related to phosphatemia. FGF-23 was higher in subjects with a history of CV disease compared to those free of such history (559.0 vs.184.0 RU/ml), adjusted to age and eGFR. CONCLUSION: Our data suggest a possible relationship between FGF-23, MMP-2 and CV disease in CKD. Potential causality of this association remains to be elucidated. (c) 2009 S. Karger AG, Basel.

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$a Fibroblast growth factor 23 and matrix-metalloproteinases in patients with chronic kidney disease: are they associated with cardiovascular disease? / $c M. Peiskerová, M. Kalousová, M. Kratochvílová, S. Dusilová-Sulková, J. Uhrová, Š. Bandúr, I.M. Malbohan, T. Zima, V. Tesař
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$a Department of Nephrology, First Faculty of Medicine, Charles University, Hradec Kralove, Czech Republic. mpeiskerova @ seznam.cz
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$a BACKGROUND: High cardiovascular risk in patients with chronic kidney disease (CKD) may be related to mineral disorder and microinflammation. Fibroblast growth factor 23 (FGF-23) is a phosphatonin and inhibitor of calcitriol synthesis, which is associated with poor prognosis in CKD patients starting dialysis. Matrix-metalloproteinases (MMP-2, MMP-9) contribute to myocardial remodeling and arterial calcification. FGF-23 and MMPs levels are altered in CKD, however, little is known about their association and relation to cardiovascular (CV) disease. METHODS: Standard laboratory parameters, plasma levels of MMP-2, MMP-9, FGF-23, PAPP-A and CV disease history were assessed in 80 patients with CKD 1-5 and 44 healthy control subjects. RESULTS: FGF-23 and MMP-2 (assessed by ELISA) were higher in CKD patients compared to controls. FGF-23 increased from CKD 3, whereas MMP-2 increased only in CKD 5. FGF-23 was positively associated with MMP-2, adjusted to age, eGFR, phosphatemia, calcitriol and parathormone. FGF-23 independently correlated with parathormone and inversely with calcitriol, whereas MMP-2 was related to phosphatemia. FGF-23 was higher in subjects with a history of CV disease compared to those free of such history (559.0 vs.184.0 RU/ml), adjusted to age and eGFR. CONCLUSION: Our data suggest a possible relationship between FGF-23, MMP-2 and CV disease in CKD. Potential causality of this association remains to be elucidated. (c) 2009 S. Karger AG, Basel.
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