Risk-benefit ratio of angiotensin antagonists versus ACE inhibitors in end-stage renal disease

Citation
Da. Sica et al., Risk-benefit ratio of angiotensin antagonists versus ACE inhibitors in end-stage renal disease, DRUG SAFETY, 22(5), 2000, pp. 350-360
Citations number
101
Categorie Soggetti
Pharmacology
Journal title
DRUG SAFETY
ISSN journal
01145916 → ACNP
Volume
22
Issue
5
Year of publication
2000
Pages
350 - 360
Database
ISI
SICI code
0114-5916(200005)22:5<350:RROAAV>2.0.ZU;2-#
Abstract
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.