FGF-23 and osteoprotegerin are independently associated with myocardial damage in chronic kidney disease stages 3 and 4. Another link between chronic kidney disease-mineral bone disorder and the heart
Author(s) -
Michelle Ford,
Edward R. Smith,
Laurie A. Tomlinson,
P. K. Chatterjee,
C. Rajkumar,
S. Holt
Publication year - 2011
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfr316
Subject(s) - medicine , fibroblast growth factor 23 , kidney disease , osteoprotegerin , arterial stiffness , cardiology , osteopontin , biomarker , endocrinology , kidney , blood pressure , parathyroid hormone , calcium , biology , activator (genetics) , receptor , biochemistry
Extra-skeletal calcification and disordered phosphate metabolism are hallmarks of chronic kidney disease-mineral bone disorder (CKD-MBD). Osteoprotegerin (OPG) and fibroblast growth factor 23 (FGF-23) are increased in chronic kidney disease (CKD) and have been associated with arterial and cardiac dysfunction and reduced survival. Troponin T (cTnT) is released from cardiac myocytes under conditions of stress and is predictive of mortality across a range of renal functions. However, the utility of this biomarker was formerly limited by the lower limit of assay detection. The introduction of a high-sensitivity assay has enabled more detailed study of myocyte stress below the previous limit of detection. We studied the association of mediators of CKD-MBD with arterial stiffness and also of these mediators and arterial stiffness with myocardial damage in patients with CKD stages 3-4.
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