Erschienen in:
01.09.2006 | Editorial Commentary
Cystatin C, kidney function and cardiovascular disease
verfasst von:
Arend Bökenkamp, Stefan Herget-Rosenthal, Regina Bökenkamp
Erschienen in:
Pediatric Nephrology
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Ausgabe 9/2006
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Abstract
Cystatin C, an endogenous low-molecular-weight marker of glomerular filtration rate, has recently been shown to be associated with future cardiovascular disease in healthy elderly populations and patients with documented atherosclerosis in a dose-dependent manner that possibly reflects a very early stage of chronic renal dysfunction. At the same time, local cystatin C deficiency has been demonstrated in atherosclerotic and aneurismal lesions, suggesting a protective role of cystatin C in the vessel wall, possibly in concert with TGF-β1. Although cystatin C is not an acute phase reactant, large epidemiological studies have documented a highly significant association between serum cystatin C and mildly increased C-reactive protein (CRP) levels, the hallmark of the chronic inflammatory state associated with atherosclerosis and chronic renal failure. Since cystatin C is produced by all nucleated cells, it is unlikely that local variations in cystatin C synthesis in diseased arteries – rather than global cystatin C production and renal elimination – should determine its serum concentration. Consequently, the present review proposes microinflammation as the unifying concept for both lines of evidence.