Studies in the general population suggest that low-grade inflammation, endothelial
dysfunction, and platelet activation are associated with an increased risk of cardiovascular
events.
Markers of inflammation, endothelial dysfunction, and platelet activation were measured
in 334 patients with chronic kidney disease (serum creatinine >1.47 mg/dL [>130 micromol/L]
at screening) and compared with 2 age- and sex-matched control groups, 1 comprising
92 patients with coronary artery disease and the other comprising 96 apparently healthy
individuals with no history of cardiovascular or kidney disease.
There was evidence of low-grade inflammation in the chronic renal impairment group
compared with healthy controls, with higher concentrations of C-reactive protein (3.70
versus 2.18 mg/L, P < 0.01) and fibrinogen (3.48 versus 2.67 g/L, P < 0.001) and lower
serum albumin concentration (41.8 versus 44.0 g/dL [418 versus 440 g/L], P < 0.001).
More severe renal impairment was associated with a trend towards higher fibrinogen
and lower albumin concentrations (both P < 0.001), although there was no association
with higher C-reactive protein level. As compared to healthy controls, plasma von
Willebrand factor (142 versus 108 IU/dL, P < 0.001) and soluble P-selectin concentrations
(57.0 versus 43.3 ng/mL, P < 0.001) were also higher in the chronic renal impairment
group. More severe renal impairment was associated with a trend towards higher levels
of von Willebrand factor (P < 0.001) and of soluble P selectin (P < 0.05).
This cross-sectional analysis demonstrates that chronic kidney disease is associated
with low-grade inflammation, endothelial dysfunction, and platelet activation, even
among patients with moderate renal impairment.