TY - JOUR
T1 - Cystatin C, kidney function and cardiovascular disease
AU - Bökenkamp, Arend
AU - Herget-Rosenthal, Stefan
AU - Bökenkamp, Regina
PY - 2006/9
Y1 - 2006/9
N2 - 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.
AB - 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.
KW - CRP
KW - Cardiovascular disease
KW - Chronic kidney disease
KW - Cystatin C
KW - Renal function test
KW - TGF-β1
UR - http://www.scopus.com/inward/record.url?scp=33746978637&partnerID=8YFLogxK
U2 - https://doi.org/10.1007/s00467-006-0192-5
DO - https://doi.org/10.1007/s00467-006-0192-5
M3 - Comment/Letter to the editor
C2 - 16838182
SN - 0931-041X
VL - 21
SP - 1223
EP - 1230
JO - Pediatric Nephrology
JF - Pediatric Nephrology
IS - 9
ER -