Inflammation is associated with carotid atherosclerosis in dialysis patients. Creed Investigators. Cardiovascular Risk Extended Evaluation in Dialysis Patients.
OBJECTIVE
To investigate the relationship between inflammatory processes and atherosclerosis in uraemic patients on chronic dialysis.


METHODS
A cross-sectional study in 138 dialysis patients (92 on haemodialysis and 46 on continuous ambulatory peritoneal dialysis).


METHODS
Serum C-reactive protein (CRP), IgG anti-Chlamydia pneumoniae antibodies, lipoprotein (a), fibrinogen and plasma homocysteine as well as the intima-media thickness and the number of atherosclerotic plaques of the carotid arteries (by Echo-Colour-Doppler) were measured in each patient


RESULTS
One hundred and eight patients had at least one plaque and 26 had more than six plaques. Serum CRP was above the upper limit of the normal range (5 mg/I) in 85 of 138 patients (62%). IgG anti-Chlamydia pneumoniae antibodies were detectable in 64% of patients (high level in 24%, intermediate in 33% and low in 7%) and undetectable in the remaining 36% of patients. In a multiple regression model age (beta=0.35), serum CRP (beta=0.23), plasma homocysteine (beta=0.19), duration of dialysis (beta=0.19) and pulse pressure (beta=0.18) were independent predictors of intima-media thickness (R=0.54, P < 0.0001). Similarly, age (beta=0.33), serum CRP (beta=0.29), plasma homocysteine (beta=0.20) and serum albumin (beta=-0.18) were independent correlates of the number of atherosclerotic plaques (R = 0.55, P < 0.0001 ). Furthermore, in smokers, the interaction serum CRP-IgG anti-Chlamydia pneumoniae antibodies was the stronger independent predictor (beta=0.43, P=0.0001) of the number of atherosclerotic plaques while no such relationship (P=0.73) was found in non-smokers.


CONCLUSIONS
In patients on chronic dialysis treatment CRP is independently associated to carotid atherosclerosis and appears at least in part to be explained by IgG anti-Chlamydia pneumoniae antibodies level. These data lend support to the hypothesis that inflammation plays a role in the pathogenesis of atherosclerosis in these patients.
Zoccali
C
C
CNR Centro Fisiologia Clinica e Divisione di Nefrologia, Ospedali Riuniti, Reggio Cal, Italy. czoccali@diel.it
Benedetto
F A
FA
Mallamaci
F
F
Tripepi
G
G
Fermo
I
I
Focà
A
A
Paroni
R
R
Malatino
L S
LS
D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000276:immunology* / Q000382:microbiology; D002690:Chlamydia Infections / Q000276:immunology*; D016993:Chlamydophila pneumoniae; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007676:Kidney Failure, Chronic / Q000276:immunology* / Q000382:microbiology / Q000628:therapy; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008567:Membranes, Artificial; D008875:Middle Aged; D010531:Peritoneal Dialysis, Continuous Ambulatory; D011237:Predictive Value of Tests; D012044:Regression Analysis; D006435:Renal Dialysis; D018615:Ultrasonography, Doppler, Color; D014511:Uremia / Q000276:immunology / Q000382:microbiology / Q000628:therapy
D000907:Antibodies, Bacterial; D007074:Immunoglobulin G; D017270:Lipoprotein(a); D008567:Membranes, Artificial; D006710:Homocysteine; D005340:Fibrinogen; D002097:C-Reactive Protein