End-stage renal disease (
ESRD) causes oxidative stress,
inflammation,
low-density lipoprotein (
LDL) oxidation,
high-density lipoprotein (HDL) deficiency and accelerated
atherosclerosis. Uptake of
oxidized LDL by macrophages results in foam cell and plaque formation. HDL mitigates
atherosclerosis via reverse
cholesterol transport and inhibition of
LDL oxidation.
ESRD heightens
LDL inflammatory activity and suppresses HDL anti-inflammatory activity. The effect of
hemodialysis on the
LDL and HDL inflammatory properties is unknown. By removing the potential
pro-oxidant/proinflammatory
uremic toxins, dialysis may attenuate
LDL inflammatory and HDL anti-inflammatory properties. Conversely, exposure to dialyzer membrane and tubing and influx of impurities from
dialysate can intensify
LDL and HDL inflammatory activities. This study examined the effect of
hemodialysis on
LDL and HDL inflammatory activities. Plasma samples were obtained from 12 normal control and 26
ESRD patients before and after
hemodialysis with (16 patients) or without (10 patients) heparinization. HDL and
LDL were isolated and tested for monocyte chemotactic activity in cultured endothelial cells.
ESRD patients had increased
LDL chemotactic activity, reduced HDL anti-inflammatory activity,
paraoxonase and
glutathione peroxidase levels, and elevated plasma
IL-6 before dialysis.
Hemodialysis partially improved
LDL inflammatory and HDL anti-inflammatory activities and enhanced patients' HDL ability to suppress their
LDL inflammatory activity. The salutary effect on
LDL inflammatory activity was significantly greater in patients dialyzed with than those without
heparin.
ESRD heightens
LDL inflammatory and impairs HDL anti-inflammatory activities.
Hemodialysis partially improves
LDL and HDL inflammatory activities. The salutary effects of
hemodialysis are in part mediated by
heparin, which is known to possess lipolytic and
antioxidant properties.