The effective treatment of hypertension is an extremely important considera
tion in patients with end-stage renal disease (ESRD). Virtually any drug cl
ass with the possible exception of diuretics - can be used to treat hyperte
nsion in the patient with ESRD. Despite there being such a wide range of tr
eatment options, drugs which interrupt the renin-angiotensin axis are gener
ally suggested as agents of choice in this population, even though the evid
ence in support of their preferential use is quite scanty.
ACE inhibitors, and more recently angiotensin antagonists, are the 2 drug c
lasses most commonly employed to alter renin-angiotensin axis activity and
therefore produce blood pressure control. ACE inhibitor use in patients wit
h ESRD can sometimes prove an exacting proposition ACE inhibitors are varia
bly dialysed, with compounds such as catopril, enalaprill lisinopril and pe
rindopril undergoing substantial cross-dialyser clearance during a standard
dialysis session. This phenomenon makes the selection of a dose and the ti
ming of administration for an ACE inhibitor a complex issue in patients wit
h ESRD.
Furthermore, ACE inhibitors are recognised as having a range of nonpressor
effects that are pertinent to patients with ESRD. Such effects include thei
r ability to decrease thirst drive and to decrease erythropoiesis. In addit
ion, ACE inhibitors have a unique adverse effect profile. As is the case wi
th their use in patients without renal failure, use of ACE inhibitors in pa
tients with ESRD can be accompanied by cough and less frequently by angione
urotic oedema. In the ESRD population, ACE inhibitor use is also accompanie
d by so-called anaphylactoid dialyser reactions.
Angiotensin antagonists are similar to ACE inhibitors in their mechanism of
blood pressure lowering. Angiotensin antagonists are not dialysable and th
erefore can be distinguished from a number of the ACE inhibitors. In additi
on, the adverse effect profile for angiotensin antagonists is remarkably bl
and, with cough and angioneurotic oedema rarely, if ever, occurring. In pat
ients with ESRD, angiotensin antagonists are also not associated with the a
naphylactoid dialyser reactions which occur with ACE inhibitors. The nonpre
ssor effects of angiotensin antagonists - such as an influence on thirst dr
ive and erythropoiesis - have not been explored in nearly the depth, as the
y have been with ACE inhibitors. Although ACE inhibitors have not been comp
ared directly to angiotensin antagonists in patients with ESRD, angiotensin
antagonists possess a number of pharmacokinetic and adverse effect charact
eristics, which would favour their use in this population.