Several clinical studies reported an increased prevalence and accelerated progression of aortic valve calcification among patients with end-stage renal disease when compared with subjects with normal kidney function. Recently, mechanisms of calcific valve degeneration have been further elucidated and many of the pathways involved could be amplified in patients with decreased renal function. In particular, calciumphosphate balance, MGP metabolism, OPG/RANK/RANKL triad, fetuin-A mineral complexes and FGF-23/Klotho axis have been shown to be impaired among patients with advanced chronic kidney disease and could play a role during vascular/valve calcification. The scope of the present review is to summarize the clinical data and the pathophysiological mechanisms potentially involved in the link between renal function decline and the progression of aortic valve disease.
Aortic valve calcification in chronic kidney disease
RATTAZZI, MARCELLO;FAGGIN, ELISABETTA;PAULETTO, PAOLO
2013
Abstract
Several clinical studies reported an increased prevalence and accelerated progression of aortic valve calcification among patients with end-stage renal disease when compared with subjects with normal kidney function. Recently, mechanisms of calcific valve degeneration have been further elucidated and many of the pathways involved could be amplified in patients with decreased renal function. In particular, calciumphosphate balance, MGP metabolism, OPG/RANK/RANKL triad, fetuin-A mineral complexes and FGF-23/Klotho axis have been shown to be impaired among patients with advanced chronic kidney disease and could play a role during vascular/valve calcification. The scope of the present review is to summarize the clinical data and the pathophysiological mechanisms potentially involved in the link between renal function decline and the progression of aortic valve disease.
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