Nephrology Dialysis Transplantation, Vol 13, Issue 90002 3-8, Copyright © 1998 by Oxford University Press
C Winearls
The need for a renewable source of erythropoietin to treat the anaemia of
chronic renal failure was first recognized in the 1960s, but cloning and
expression of the human gene was not achieved until 1983. Clinical testing
of recombinant human erythropoietin (rHuEPO) began in 1985, leading to the
first licence as a therapeutic agent in 1988. The first clinical trials
showed that an intravenous dose requirement of about 200 IU/kg/week would
increase haemoglobin concentrations to 10-12 g/dl in >90% of
haemodialysis patients. Subcutaneous administration has subsequently been
found to be effective, and may allow lower maintenance doses. It is now the
route of choice in Europe, but not the USA. The best marker of benefit of
the introduction of r-HuEPO is the reduction in need for regular blood
transfusions. A marked improvement in anaemia-related symptoms has been
clearly demonstrated. The most important factor in optimizing the response
to r-HuEPO is iron supply. The marrow should be stimulated slowly, to allow
mobilization of iron stores. Functional or absolute iron deficiency should
be pre-empted by regular iron supplementation. It is also important to
recognize resistant states induced by inflammation and bleeding, and to
exclude severe hyperparathyroidism, aluminium overload and other
haematological diseases. The most important adverse events associated with
r-HuEPO are increased blood pressure and a possible increased risk of
access failure. These are, however, challenges to improve practice, not
reasons to avoid the use of r-HuEPO.Key words:
anaemia, chronic renal failure, erythropoietin, iron
ORIGINAL ARTICLES
Recombinant human erythropoietin: 10 years of clinical experience
Renal Unit, The Churchill, The Oxford Radcliffe Hospital NHS Trust, Headington, Oxford OX3 7LJ, UK
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