Cardiovascular complications caused by an accelerated atherosclerotic disea
se represent the largest single cause of mortality in chronic renal failure
patients. The rapidly developing atherosclerosis of the uremic syndrome ap
pears to be caused by a synergism of different mechanisms, such as malnutri
tion, oxidative stress and genetic factors. Recent studies provide evidence
that chronic inflammation plays an important role in the pathogenesis of c
ardiovascular diseases. Elevated serum levels of plasma C-reactive protein
(CRP) are associated with an increased risk of experiencing myocardial infa
rction and sudden cardiac death in apparently healthy subjects. Several rec
ently published pa pers have confirmed this strong association between CRP
and the extent and severity of the atherosclerotic processes. In patients a
ffected by predialytic renal failure, increased levels of CRP and interleuk
in (IL)-6 were recorded in 25% of our population; CRP and IL-6 were inverse
ly related with renal function. These data suggest the activation - even in
the predialytic phase of renal failure - of mechanisms known to contribute
to the enhanced cardiovascular morbidity and mortality of the uremic syndr
ome. In recent years we have investigated the hypothesis that the chronic i
nflammatory state of the uremic patient could at least in part be due to th
e dialytic technique. We provide evidence suggesting that the increase of C
RP in stable dialytic patients may be due to the stimulation of monocyte/ma
crophage by backfiltration of dialysate contaminants. Copyright (C) 2000 S.
Karger AG, Basel.