Circulating blood leukocytes have short life expectancies and end their liv
es by committing programmed cell death or apoptosis. Apoptosis is an active
form of cell death that is initiated by a number of stimuli and is intrica
tely regulated. Apoptosis in both excessive and reduced amounts has patholo
gical implications. Evidence suggests that apoptosis may play a role in the
pathophysiology of immune dysfunction in uremia. Indeed, accelerated progr
ammed cell death has been observed in lymphocytes, monocytes, and polymorph
onuclear leukocytes among patients with chronic renal failure. This may be
due in part to the retention of uremic toxins. The aim of this article is t
o review the evidence for accelerated leukocyte apoptosis, key regulatory a
poptotic pathways, and the possible role of this highly organized process i
n the pathogenesis of immune dysfunction in uremia.