The anemia of renal failure is caused by the lack of sufficient quantities
of endogenous erythropoietin. With the availability of recombinant human er
ythropoietin (rHuEPO), however, it has become apparent that to achieve a gi
ven target, hematocrit requires proper management of iron replacement, as w
ell as the administration of rHuEPO. Iron deficiency, either absolute or fu
nctional, will occur in most, if not all, patients on hemodialysis receivin
g rHuEPO because of the increased demand for iron driven by the accelerated
erythropoiesis that occurs with exogenous rHuEPO administration, coupled w
ith ongoing blood losses from dialyzer and tubing, blood sampling, gastroin
testinal blood loss, and blood losses at the time of dialysis needle placem
ent and removal. Blood loss is less of a problem in patients on peritoneal
dialysis, but poor iron intake and increased demand for iron are also seen,
the latter in patients receiving rHuEPO. It is essential, therefore, for r
enal health professionals to understand iron metabolism in dialysis patient
s in order to properly balance the therapy of renal anemia with rHuEPO and
supplemental iron.