Blood-dialyzer interaction in hemodialysis has the potential to activate mo
nonuclear cells leading to the production of inflammatory cytokines. The ex
tent of activation is dependent on the dialyzer material used and is consid
ered an index of biocompatibility. Cytokines. such as interleukin-1 beta (I
L-1 eta), tumor necrosis factor-alpha (TNF-alpha), and IL-6, may induce an
inflammatory state and are believed to play a significant role in dialysis-
related morbidity. The interleukin hypothesis suggests that the release of
proinflammatory cytokines acts as an underlying pathophysiologic event in h
emodialysis-related acute manifestations, such as fever and hypotension. Ne
vertheless, a cytokine overproduction may alter sleep pattern in chronic he
modialyzed patients, thus explaining the presence of sleep disorders in the
se patients. A potential role of cytokines in chronic-related morbidity has
also been suggested. High levels of some inflammatory cytokines are often
associated with anemia caused by hyporesponsiveness to erythropoietin. Cyto
kine production may also play a relevant role in bone remodeling by regulat
ing osteoblast/osteoclast cell functions and parathyroid hormone (PTH). Fin
ally, cytokine release may have a long-term deleterious effect on mortality
of uremic patients by altering immune response and increasing susceptibili
ty to infections. Bioincompatibility of dialytic membranes may also contrib
ute to malnutrition in dialysis patients by increasing the monocyte release
of catabolic cytokines such as TNF-alpha and IL-6. Bioincompatible dialyti
c treatment may induce an inappropriate monocyte activation and cytokine pr
oduction, which, in turn, may mediate some of the immune and metabolic dysf
unction associated with hemodialysis. The use of biocompatible dialytic mem
branes appears to reduce the monocyte activation and to improve the surviva
l of hemodialysis patients.