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Cystatin C, kidney function and cardiovascular disease

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An Erratum to this article was published on 01 March 2007

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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.

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Fig. 1
Fig. 2

Change history

  • 01 March 2007

    In our review, we stated that C-reactive protein (CRP) levels were not adjusted for in the Cardiovascular Health Study. As can be seen from the legend for Table 1 of our paper, CRP was well included in the various analyses published from the Cardiovascular Health Study data.

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Conflict of interest statement

A.B. received honoraria from Dade Behring, Marburg, Germany and DAKO, Glostrup, Denmark. S. H. received honoraria from Dade Behring, Marburg, Germany.

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Bökenkamp, A., Herget-Rosenthal, S. & Bökenkamp, R. Cystatin C, kidney function and cardiovascular disease. Pediatr Nephrol 21, 1223–1230 (2006). https://doi.org/10.1007/s00467-006-0192-5

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