Nephrol Dial Transplant (1999) 14: 2798-2800
© 1999 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
C-reactive protein and coronary artery disease—what is the link?
Department of Medicine, Division of Cardiology, University of Ulm and 1 Department of Medicine, Division of Nephrology, University of Würzburg, Germany
Correspondence and offprint requests to: C. Wanner MD, Department of Medicine, Division of Nephrology, University Hospital, Josef-Schneider-Strasse 2, D-97080 Würzburg, Germany. E-mail: c.wanner@medizin.uni-wuerzburg.de.
Evidence for inflammation in atherosclerosis
Inflammation of the vessel wall is now considered to play an essential role in the initiation and progression of atherosclerosis [1], and also in its final steps, i.e. plaque erosion or fissure, and eventually plaque rupture [2]. This notion is based on classical pathological studies showing the presence of inflammatory cells, such as monocyte-derived macrophages, T-lymphocytes, and mast cells not only at the site of rupture or superficial erosion [3] but rather at every stage of the disease, even in the very early lesions, the so-called fatty streaks. These morphologic changes are preceded by dysfunction of activated endothelial cells that produce so called adhesion molecules (ICAM-1, E-selectin) that interact with inflammatory cells [4]. The ability of monocyte-derived macrophages to secrete various cytokines (IL-1, IL-6, TNF-
),
C-reactive protein (CRP)
CRP is a long-term predictor of cardiovascular risk
CRP in acute coronary syndromes
CRP in the renal patient
Should we include CRP in the risk profile?
Hypothesis and future perspectives
It is unclear whether or not an inflammatory protein such as CRP is involved causally in atherosclerosis or merely represents a marker of disease
We need to know the underlying factor(s) that turn on the acute phase response
If inflammation were to play an important causal role in atherosclerosis, should it become a therapeutic target?
Summary and conclusion
References
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