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2017 ; 28
(4
): 1278-1285
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Arterial and Cellular Inflammation in Patients with CKD
#MMPMID27799487
Bernelot Moens SJ
; Verweij SL
; van der Valk FM
; van Capelleveen JC
; Kroon J
; Versloot M
; Verberne HJ
; Marquering HA
; Duivenvoorden R
; Vogt L
; Stroes ES
J Am Soc Nephrol
2017[Apr]; 28
(4
): 1278-1285
PMID27799487
show ga
CKD associates with a 1.5- to 3.5-fold increased risk for cardiovascular disease.
Both diseases are characterized by increased inflammation, and in patients with
CKD, elevated C-reactive protein level predicts cardiovascular risk. In addition
to systemic inflammation, local arterial inflammation, driven by monocyte-derived
macrophages, predicts future cardiovascular events in the general population. We
hypothesized that subjects with CKD have increased arterial and cellular
inflammation, reflected by (18)F-fluorodeoxyglucose ((18)F-FDG) positron emission
tomography computed tomography (PET/CT) of the arterial wall and a migratory
phenotype of monocytes. We assessed (18)F-FDG uptake in the arterial wall in 14
patients with CKD (mean±SD age: 59±5 years, mean±SD eGFR: 37±12 ml/min per 1.73
m(2)) but without cardiovascular diseases, diabetes, or inflammatory conditions
and in 14 control subjects (mean age: 60±11 years, mean eGFR: 86±16 ml/min per
1.73 m(2)). Compared with controls, patients with CKD showed increased arterial
inflammation, quantified as target-to-background ratio (TBR) in the aorta
(TBR(max): CKD, 3.14±0.70 versus control, 2.12±0.27; P=0.001) and the carotid
arteries (TBR(max): CKD, 2.45±0.65 versus control, 1.66±0.27; P<0.001).
Characterization of circulating monocytes using flow cytometry revealed increased
chemokine receptor expression and enhanced transendothelial migration capacity in
patients with CKD compared with controls. In conclusion, this increased arterial
wall inflammation, observed in patients with CKD but without overt
atherosclerotic disease and with few traditional risk factors, may contribute to
the increased cardiovascular risk associated with CKD. The concomitant elevation
of monocyte activity may provide novel therapeutic targets for attenuating this
inflammation and thereby preventing CKD-associated cardiovascular disease.
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