Cystatin C, kidney function and cardiovascular disease.
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-beta1. 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.
Bökenkamp
Arend
A
Herget-Rosenthal
Stefan
S
Bökenkamp
Regina
R
D000818:Animals; D015415:Biomarkers; D002318:Cardiovascular Diseases / Q000378:metabolism* / Q000503:physiopathology*; D055316:Cystatin C; D015891:Cystatins / Q000502:physiology*; D005919:Glomerular Filtration Rate; D006801:Humans; D007668:Kidney / Q000502:physiology* / Q000503:physiopathology
D015415:Biomarkers; C525030:CST3 protein, human; D055316:Cystatin C; D015891:Cystatins