It is well established that ACE inhibitors should be avoided in patients with critical renal artery stenosis. In contrast, this is not as well established with respect to angiotensin II antagonists. Over the last years a few cases have shown that renal function may be impaired if the angiotensin II antagonist losartan is used in patients with renal artery stenosis [
1,
2,
3,
4] but two of these cases were in the special situation of kidney transplants [
3,
4]. To our knowledge we are the first to report a case of renal impairment induced by the angiotensin II antagonist candesartan. Subsequent to the introduction of losartan, several other angiotensin II blockers have been marketed over the last couple of years and differences in receptor affinity and kinetics are reported. Therefore, our case supports the thought that caution should be shown using other types of angiotensin II antagonists. As mentioned in the introduction several differences exist between ACE inhibitors and angiotensin II, AT
1-receptor antagonists. Therefore, differences with regard to interference with renal function and thereby when the compound should be avoided could exist. From a theoretical point of view however, one would expect that both principles of blockade should be avoided in renal artery stenosis. The mechanism of the renin-angiotensin system in regulation of renal function is believed primarily to be due to the effect of angiotensin II on the efferent arteriolar tone keeping the pressure relatively constant in the glomerulus and thereby keeping GFR constant over a wide range of perfusion pressures,
i.e. systemic BP. However, the differential effect on
e.g. bradykinin, which is a vasodilator and also have other actions, could in theory make the two types of blockade clinically different. At present, the relative risk of precipitating renal failure by using the different compounds is unsettled. Thus in one case renal function deteriorated following both the ACE inhibitor enalapril and losartan [
1]. In contrast, another case-report observed deterioration of renal function during enalapril treatment but no effect of subsequent losartan treatment [
5]. Conversely, in a study comparing the usefulness of the ACE inhibitor captopril and losartan renography for detection of renovascular hypertension it was in a single case found that losartan but not captopril induced a fall in renal function in a kidney with more than 80% renal artery stenosis [
6].
Our case also demonstrates that renography is an easy way to examine and follow patients with deterioration of renal function during treatment with angiotensin II antagonists or ACE inhibitors. When of relevance, the additional use of angiography and selective renin measurements add further evidence for the reason for renal impairment.
We conclude, that further studies are needed to demonstrate potential differences in the use of ACE inhibitors and angiotensin II antagonists in patients with suspected renal artery stenosis. Until then, both compounds should be avoided in this category of patients.