ANGIOTENSIN-CONVERTING ENZYME INHIBITOR-INDUCED RENAL DYSFUNCTION IN ATHEROSCLEROTIC RENOVASCULAR DISEASE

Citation
Pjg. Vandeven et al., ANGIOTENSIN-CONVERTING ENZYME INHIBITOR-INDUCED RENAL DYSFUNCTION IN ATHEROSCLEROTIC RENOVASCULAR DISEASE, Kidney international, 53(4), 1998, pp. 986-993
Citations number
63
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00852538
Volume
53
Issue
4
Year of publication
1998
Pages
986 - 993
Database
ISI
SICI code
0085-2538(1998)53:4<986:AEIRDI>2.0.ZU;2-7
Abstract
Ischemic nephropathy due to bilateral renovascular disease (RVD) is in creasingly recognized as cause of end-stage renal failure in the elder ly, but a reliable non-invasive method of detection is not available. Angiotensin converting enzyme inhibition (ACEi) may impair renal funct ion in such patients, but a prospective study of its diagnostic validi ty has not been undertaken. We studied the: effects of controlled expo sure to ACEi on plasma creatinine in 108 patients at risk for severe b ilateral atherosclerotic RVD, and compared the findings with subsequen t angiography. ACEi was given for two weeks, or, to avoid acute renal failure, for four days If plasma creatinine had increased by 20% or mo n. If after two weeks of ACEi plasma creatinine had not increased by g reater than or equal to 20%, while blood pressure was still elevated, plasma creatinine was remeasured after blood pressure control by addit ion of diuretics. The severity of RVD was scored by the stenosis grade of the best perfused kidney. Fifty-two patients had severe bilateral RVD, defined as greater than or equal to 50% stenosis to both kidneys (N = 23) or a solitary functioning kidney (N = 29). Of the others, 21 had less severe bilateral RVD, 20 unilateral RVD, and 15 no apparent R VD. Basal plasma creatinine was higher in severe bilateral RVD (median 170 mu mol/liter, range 85 to 654 mu mol/liter) than in the others (1 22 mu mol/liter, 62 to 675 mu mol/liter; P < 0.01), but not discrimina tive doe to a large variability. The increase during ACEi was correlat ed with the degree of RVD (r = 0.53, P < 0.001). In 69 patients ACEi c aused at least a 20% increase in plasma creatinine, in 26 cases by fou r days. in 31 after two weeks, and in 12 only after blood pressure con trol by diuretics. Among these were all 52 patients xith severe bilate ral RVD, 15 of the 41 patients with lesser forms of RVD, and two with normal renal arteries. Thus, In this selected population the criterion of greater than or equal to 20% rise in plasma creatinine upon ACEi w as 100% sensitive to detect severe bilateral RVD, while its specificit y was 70%. No case of acute renal failure was encountered, and plasma creatinine always recovered after stopping ACEi. In conclusion, contro lled elrposure to ACEi in these patients is safe, and ACEi-induced inc rease in plasma creatinine is a very sensitive detector of severe bila teral RVD in a high risk population.