Patients with end-stage renal failure present with various debilitatin
g forms of renal osteodystrophy characterized either by high bone turn
over with or without mineralization defect or low bone turnover, that
is, adynamic bone disease. Alterations in parathyroid hormone and calc
itriol production do not completely account for the abnormalities in b
one turnover. This suggest that other factors or mediators, or both, a
re involved in the regulation of bone turnover. Among them, the cytoki
ne systems are of particular interest because of the following: cytoki
ne production is altered in uremic patients; there are interactions be
tween parathyroid hormone, calcitriol, and cytokines; and cytokines mo
dulate bone cell number or activity, or both. Preliminary results of d
irect assessment of cytokines in bone of uremic patients are promising
. Future research in this field should advance our knowledge of the in
tricate mechanisms that regulate bone turnover in renal osteodystrophy
. This could provide a basis for better strategies in the control of b
one abnormalities in uremic patients.