Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two female patients who developed acute renal failure secondary to the use of angiotensin converting enzyme (ACE) inhibitors for hypertension are presented. None had renal artery stenosis on angiography or duplex doppler ultrasound examination. A 66 year old patient with a single functioning kidney recovered basal renal function; the other patient, aged 77 years, remained with a permanent severe renal damage. Risk factors were advanced age, mild chronic renal failure due to nephrosclerosis and diuretic use. We conclude that acute renal failure related to ACE inhibitors may be severe and can occur even in patients without renal artery stenosis. Diuretics, associated to ACE inhibitors, should be prescribed with caution, specially in older hypertensive patients with pre-existing chronic renal failure. Diabetic patients are at special risk due to the high incidence of small vessel disease in them.
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PMID:[Acute renal insufficiency secondary to the use of angiotensin converting enzyme inhibitors in 2 patients without renal artery stenosis]. 134 Sep 49

Treatment with an angiotensin converting enzyme (ACE) inhibitor can result in acute renal failure in patients with a renal artery stenosis. In the present study the effects of the selective nonpeptide angiotensin II antagonists, SK&F 108566 ((E)-alpha-[[2-Butyl-1-[(4-carboxyphenyl)methyl]-1H-imidazol-5-yl] methylene]-2-thiophenepropanoic acid) and EXP3174 (2-n-Butyl-4-chloro-1-[(2'-(1H-tetrazol-5-yl)-biphenyl-4-yl) methyl]imidazole-5-carboxylic acid hydrochloride) (the active metabolite of DuP 753, losartan) were compared with the ACE inhibitor, captopril, in the anesthetized dog which had been uninephrectomized and the remaining renal artery clamped to reduce renal blood flow (RBF) by approximately 50%. All three agents resulted in dose-dependent reductions in mean arterial pressure (MAP), glomerular filtration rate (GFR) and RBF. The maximum responses to captopril and SK&F 108566 were similar with MAP, RBF and GFR all decreasing approximately 30%. EXP3174 also resulted in decreases in GFR and RBF of approximately 30%; however, there was a smaller (approximately 17%) decrease in MAP. The data indicate that the possible bradykinin enhancing activity of ACE inhibitors may not provide any moderating activity of ACE inhibitor-induced reduction in GFR observed in dogs with a renal artery stenosis.
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PMID:Effect of captopril and the nonpeptide angiotensin II antagonists, SK&F 108566 and EXP3174, on renal function in dogs with a renal artery stenosis. 143 81

In order to study why the diagnostic sensitivity of 123I-hippurate renography for a renal artery stenosis is improved by angiotensin converting enzyme (ACE-) inhibition we used the model of the conscious chronically instrumented two-kidney, one-clip Goldblatt hypertensive dog. Urine flow (UV), renal blood flow (RBF), glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured (with constant infusion of 125I-iothalamate and 131I-hippurate, respectively) for both kidneys separately before and after a bolus injection of a mild unilateral renal artery stenosis (approximately 30% reduction of RBF). During ACE-inhibition, there were remarkable falls in poststenotic GFR (from 37 +/- 5 to 4 +/- 2 ml/min, p less than 0.05), ERPF (from 111 +/- 13 to 21 +/- 10 ml/min, p less than 0.05) and UV (from 0.86 +/- 0.15 to 0.075 +/- 0.045 ml/min, p less than 0.05), whereas RBF of the poststenotic kidney slightly increased (from 193 +/- 18 to 237 +/- 27 ml/min, p less than 0.05). The concentration of hippurate and thalamate in the blood remained remarkably constant while the excretion of the tracers by the poststenotic kidney diminished and renal retention of 123I-hippurate was seen on the renogram. In 2 dogs, the experiments were repeated during mannitol infusion. In that situation, there was a much smaller decrease of poststenotic UV and GFR whereas ERPF even showed a small increase comparable to the RBF changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in renal function induced by ACE-inhibition in the conscious two-kidney, one-clip Goldblatt hypertensive dog. 155 9

Antihypertensive therapy influences kidney function by different mechanisms depending on the mode of action of the drug used. The GFR is improved by calcium entry blockers and ACE inhibitors, unaffected by vasodilators, alpha-blockers and centrally acting sympatholytics and impaired by beta-blockers. The same is true for renal blood flow and is due to changes of renal vascular resistance. Renal sodium excretion is impaired mostly by vasodilators, by alpha-blockers, sympatholytics and beta-blockers; in contrast, calcium entry blockers and ACE inhibitors acutely induce natriuresis. The RAAS is stimulated by vasodilators, unaffected by alpha-blockers and sympatholytics and suppressed by beta-blockers. Plasma catecholamines are stimulated by vasodilators and suppressed by centrally acting sympatholytics and unaffected by the others. Induction of acute renal functional impairment is reported for ACE inhibitors under conditions of compromised renal perfusion pressure such as in renal artery stenosis. These data from the literature reviewed are supported by our own experimental data on sodium balance under different drugs and micropuncture data in experimental renal artery stenosis. To achieve effective antihypertensive treatment with a low profile of side effects, careful monitoring of renal function seems to be mandatory.
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PMID:Influence of antihypertensive therapy on renal function. 159 4

The Authors describe a clinical case of a patient affected by arterial hypertension of severe degree (IV grade OMS) that during therapy with ACE inhibitors and diuretics developed acute renal failure that reversed after stopping treatment. The clinical course was quite similar to acute renal failure induced by ACE inhibitors and diuretics in patient with bilateral renal artery stenosis. In interpreting the pathogenesis, the Authors suppose, beside a reductions of effective plasma flow, the coexistence of hyalinosis of renal arterioles. They underline the necessity of monitoring renal function at least in the first weeks of therapy when a treatment with ACE inhibitors and diuretics is started especially in patients with hypertension of high degree and/or reduced renal function.
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PMID:[Acute renal failure caused by treatment with diuretics and ACE inhibitors in the absence of renal artery stenosis]. 163 Jun 98

Captopril radionuclide test (CRT) has been introduced in clinical practice as a screening test for renovascular hypertension, since it allows the detection of the decrease of glomerular filtration rate that may be induced by angiotensin converting enzyme inhibition (25 mg oral captopril) in kidneys ipsilateral to a renal artery stenosis. However, due to the low prevalence of the disease, experiences in single centers may hardly satisfy the need for representative series of patients to validate the test. Nineteen centers participated in a collaborative study (CRT European Multicenter Study) that collected data from 424 patients. Here we report on the first results obtained by inspective renographic analysis. The captopril radionuclide test greatly potentiated the diagnostic performance of conventional renography and the accuracy was maximal when relying simply on postcaptopril findings alone. Specificity was 84.1% in the overall population and 91.8% in uncomplicated patients without nephropathy and renal insufficiency. Taking into account the sole arteriographic diagnosis, sensitivity was 73.2% or 90.7% for the subjects with unilateral or bilateral stenosis and an angiographic degree of stenosis greater than or equal to 70%. On the other hand, when a successful outcome of blood pressure after revascularization or nephrectomy was considered as the gold standard for the diagnosis of renovascular hypertension, a high sensitivity was obtained (92.7%). Moreover, the test became negative after intervention in the great majority (88%) of patients who had a positive preintervention CRT and a normalization of blood pressure after revascularization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:European Captopril Radionuclide Test Multicenter Study. Preliminary results. Inspective renographic analysis. The European Captopril Radionuclide Test Multicenter Study Group. 177 83

The effect of angiotensin converting enzyme (ACE) inhibition on the sensitivity of radionuclide renography in the diagnosis of a unilateral renal artery stenosis was tested both in a conscious dog model and in the human situation. ACE inhibition (10 mg enalaprilic acid, intravenously) markedly improved the sensitivity of [123I]hippuran renography in 10 renovascular hypertensive dogs with a mild to moderate unilateral renal artery stenosis from 50 to 100%. This improved sensitivity was due to an ACE-inhibition-induced delayed tracer handling at the stenotic side without an appreciable change in the renographic curve at the contralateral side. A similar phenomenon was observed in 15 hypertensive patients with an angiographically proved unilateral renal artery stenosis. Both [123I]hippuran and 99mTc-diethylenetriaminepentaacetic acid (DTPA) handling was delayed on the stenotic side after oral enalapril treatment. However, only a moderate increase in sensitivity was observed comparing control renograms to ACE-inhibition renograms: from 87 to 93% for hippuran, and from 60 to 86% for DTPA. Eight of these 15 patients underwent either surgery or angioplasty resulting in a successful correction of the stenosis. Hypertension was more or less cured in five patients. Each of these patients had shown an ACE-inhibition-induced change in the renogram at the stenotic side, suggesting that such a response may predict the curability of the hypertension. However, of the three patients that showed no blood pressure change upon successful revascularization, two showed a positive ACE-inhibition renogram. In conclusion, in an ideal setting as obtained in animal experiments, ACE inhibition improves the sensitivity of renographic studies to 100%. However, its value in the clinical setting needs more standardization.
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PMID:The mechanism and diagnostic value of angiotensin I converting enzyme inhibition renography. 177 88

The most common curable cause of high blood pressure is renovascular hypertension. Although hypertension is common in the United States, only a minority, approximately 1%, of patients have a renovascular cause. Using clinical criteria, a subgroup of these patients can be selected in which the prevalence of renovascular hypertension will be approximately 15%. In these selected patients, it is appropriate to proceed to a radiographic screening modality to look for a significant renal artery stenosis. The choice of modality should reflect the strengths and expertise of each specific institution. Hypertensive urography is no longer recommended for screening. Excellent results have been reported with intravenous DSRA in institutions where a strong interest in this procedure exists. Furthermore, intravenous DSRA is easily coupled with the collection of renal vein samples for renin assay. Intravenous DSRA, however, has not maintained widespread use. Although the radionuclide renogram is no longer adequate as a radiographic screening tool, stimulation with an ACE inhibitor, such as captopril or enalaprilat, may produce excellent results. In many institutions, this is the most appropriate examination. Furthermore, it is relatively noninvasive. Merely detecting a significant renal artery stenosis does not, however, mean the patient has renovascular hypertension. Both hypertension and a renal artery stenosis may be present and not be causally related. Because renovascular hypertension is, at least initially, renin mediated, the demonstration of increased renin production by the ipsilateral kidney should confirm renovascular hypertension. Prospective application of these results to patients undergoing revascularization techniques, however, has been disappointing. This may be related to problems in patient preparation, sample collection, renin assay, or even the physiology of chronic hypertension, which is incompletely renin mediated. Thus, offering revascularization only to those patients with lateralizing renal vein renins is not appropriate. If radiographic screening is limited to those patient at greatest likelihood for a renovascular etiology, intra-arterial DSRA or conventional arteriography may be used. These techniques most reliably detect renal artery stenosis. Their main disadvantage lies in their relatively invasive nature, as an arterial puncture is required. The poor predictive value of selective RVRRs implies that revascularization may be attempted without awaiting those results. If percutaneous transluminal renal angioplasty can be performed with a satisfactorily low complication rate, both the diagnostic and the interventional procedure may be undertaken at the same setting. It is expected that further refinements in these diagnostic procedures, particularly with the use of stimulating drugs such as ACE inhibitors, will lead to further improvement in the diagnostic results.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Screening for renovascular hypertension. 182 6

We treated 94 patients by percutaneous transluminal angioplasty (PTA) for renal artery stenosis (RAS). Prior to PTA, a renogram during angiotensin converting enzyme (ACE) inhibition with captopril was performed, but the result did not influence the decision to treat. The parenchymal time activity curves were judged by visual interpretation. Of the 94 patients, 51 had unilateral and 43 bilateral RAS. In 17 patients with bilateral RAS, PTA could be performed only in the least affected kidney; because of this the effect of PTA on their blood pressure could not be evaluated. Of the remaining 77 patients, a positive captopril renogram was seen in all 31 cured patients, in 22 of the 27 patients with improvement, and in six of the 19 patients with no change of their blood pressure. The sensitivity of the tests for cure and improvement of the blood pressure was 91% (53/58 patients) for all patients, 95% in patients with unilateral RAS (35/37), and 86% (18/21 patients) in patients with bilateral RAS, bilaterally treated. In 18 patients with a negative captopril renogram the blood pressure improved in five, and did not change in 13 patients. The success of PTA in patients with a negative captopril renogram was so poor that we feel it would have been better not to have performed angiography and PTA at all. In conclusion, captopril renography is a useful investigation in assessing the likelihood of blood pressure reduction after PTA of renal artery stenosis.
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PMID:Captopril renography and the effect of percutaneous transluminal angioplasty on blood pressure in 94 patients with renal artery stenosis. 183 91

The RAS is part of an extremely powerful feedback system for long-term control of blood pressure and volume homeostasis. Disturbances that tend to lower blood pressure, such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due, in large part, to the combined actions of ANGII and reduced arterial pressure. In response to increased sodium intake, decreased ANGII formation greatly amplifies the effectiveness of pressure natriuresis, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium retaining effects of ANGII necessitate increased blood pressure to maintain sodium balance via pressure natriuresis. Because the RAS is so powerful in regulating blood pressure, blockade of the system with ACE inhibitors offers a powerful therapeutic tool in diseases such as hypertension and congestive heart failure. The control of sodium excretion and blood pressure by ANGII is exerted through multiple intrarenal as well as extrarenal effects, including stimulation of aldosterone secretion, which can influence renal excretion. Current evidence suggests that the intrarenal effects of ANGII are quantitatively more important than those mediated by aldosterone in controlling blood pressure and renal excretion. The most important intrarenal effects of ANGII include efferent arteriolar constriction as well as direct effects on sodium transport. The constrictor effect on efferent arterioles also is important in preventing reductions in GFR in circumstances associated with impaired renal perfusion. Therefore blockade of ANGII formation in circumstances such as renal artery stenosis may caused marked reductions in GFR. However, in many patients efferent arteriolar vasodilation caused by ANGII blockade may not lower GFR markedly because of other autoregulatory mechanisms that compensate by causing parallel reductions in afferent arteriolar resistance. In these individuals, chronic ACE inhibition may prove to be beneficial in slowing the progression of renal disease because a reduction in glomerular hydrostatic pressure may help to prevent glomerular damage.
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PMID:The renin-angiotensin system: renal actions and blood pressure regulation. 187 29


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