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)

We report a case whose renal failure was due to malignant hypertension and in whom steroid facilitated the recovery of renal function. The patient, a 41-year-old man, was admitted to our hospital because of malaise and macrohematuria. On admission, his blood pressure was 270/160 mmHg. The plasma renin activity (PRA) and aldosterone were markedly elevated. Chest X-ray, echo cardiography and electrocardiogram revealed marked hypertrophy. Hypertensive retinopathy and arteriosclerotic change were noted on ophthalmoscopy. Because of renal dysfunction (blood urea nitrogen 45.6 mg/dl, serum creatinine 4.9 mg/dl with massive proteinuria and increased FENa, renal biopsy was performed on the 8th clinical day. The specimens showed slight proliferation of mesangial cells with mesangiolysis and interstitial cell infiltration, in addition to marked arteriosclerosis and partial collapse of the glomerular tuft. After the administration of a Ca antagonist and angiotensin converting enzyme inhibitor (ACE-I), his mean blood pressure decreased to 100-130 mmHg, and urinary protein decreased as well. Nevertheless, renal dysfunction remained unchanged during the following 3 weeks. Thus, prednisolone (PSL, 30 mg/day) was administered on the 22nd clinical day and renal function improved thereafter without a significant change in blood pressure. The improved renal function was maintained after PSL tapered off on the 184th clinical day. It is suggested that PSL might be the therapy of choice in malignant hypertension, when the renal function has not been improved by anti-hypertensive treatment alone.
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PMID:[A case of malignant hypertension in whom steroid improved renal function]. 1065 31

Most studies on the antiproliferative action of angiotensin converting enzyme inhibitors (ACEI) were performed in a rat hypertensive remnant kidney model with 5/6 kidney ablation which raised objections about the antihypertensive effect of ACEI and the influence of other antihypertensive drugs administered to remnant kidney control rats. To prevent these objections, a normotensive 4/6 remnant kidney model was elaborated and a subantihypertensive dosage of enalapril was used to evaluate its antiproliferative action. Subtotally nephrectomized rats (Nx) markedly increased the remnant kidney weight during a 4-week period and this rise was prevented by the treatment with enalapril (NxE) (Nx +297+/-35 mg vs. sham-operated +145+/-32 mg, p<0.001; NxE +154+/-35 mg vs. Nx p<0.001). While collagen concentration in the kidney cortex was not increased in sham-operated rats (Sham) in comparison with the control group (Ctrl) at the beginning of the study, the subsequent increase was significant in the Nx group and enalapril did not attenuate this increase (Sham 148+/-5 mg/100 g w.w. vs. Nx 164+/-2 mg/100 g w.w., p<0.01; NxE 161+/-4 mg/100 g w.w. vs. Sham p<0.05). The tubular protein/DNA ratio increase, which was significant in the Nx group, was inhibited by enalapril (Nx 26.2+/-10.5 vs. NxE 15.3+/-2.6, p<0.05). The protein/DNA ratio was much lower in glomeruli, with no significant changes in either the Nx or NxE groups. Serum urea concentrations were slightly higher in the Nx group than in the sham-operated group, but markedly elevated in the NxE group (Nx 10.71+/-0.76 mmol/l vs. Sham 6.10+/-0.33 mmol/l, p<0.001; NxE 28.9+/-2.6 mmol/l vs. Sham p<0.001). Creatinine concentrations in the Nx group were increased in comparison with the sham-operated group and markedly increased in the NxE group (Nx 63.7+/-3.56 micromol/l vs. Sham 37.2+/-2.84 micromol/l, p<0.001; NxE 107.0+/-5.2 micromol/l vs. Sham p<0.001). The clearance of creatinine was lower in the Nx group than in the sham-operated group and was markedly reduced in the NxE group (Nx 0.89+/-0.06 ml/min.g kidney wt. vs. Sham 1.05+/-0.16 ml/min x g kidney wt., p<0.01; NxE 0.58+/-0.029 ml/min x g kidney wt. vs. Sham, p<0.001). Enalapril improved proteinuria in comparison with the Nx group (NxE 5.6+/-0.6 mg/24 h vs. Nx 16.1+/-3.4 mg/24 h, p<0.05). Thus remnant kidney proliferation is substantial even in normotensive rats. It includes both proliferation and collagen accumulation with partial recovery of kidney weight and function, but is accompanied by enhanced proteinuria. Enalapril attenuates the proliferation and decreases proteinuria but prolongs kidney function recovery.
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PMID:Enalapril in subantihypertensive dosage attenuates kidney proliferation and functional recovery in normotensive ablation nephropathy of the rat. 1078 7

We have investigated the effects of benidipine (hydrochloride), a calcium antagonist, against ischaemic acute renal failure in rats. Using histological examination, we studied whether the inhibition of apoptosis was associated with the protective effects of benidipine on the ischaemic renal injury. Acute renal failure was induced by the unilateral clamping of the left renal artery for 60 min, followed by reperfusion and contralateral nephrectomy. Drugs were given intravenously 5 min before the unilateral clamping. Prophylactic administrations of benidipine (10 microg kg(-1), i.v.) significantly ameliorated the development of renal failure as estimated by the measurements of serum creatinine and blood urea nitrogen 24 h after the reperfusion. Amlodipine (besilate, 100 and 300 microg kg(-1), i.v.) tended to attenuate renal dysfunction. Lisinopril (300 and 1000 microg kg(-1), i.v.), an angiotensin converting enzyme inhibitor, was ineffective in this acute renal failure model. Histological examination using the terminal transferase-mediated dUTP-biotin nick end-labelling (TUNEL) method to detect apoptotic cells revealed that the TUNEL-positive tubular epithelium was prominent in the renal cortex 24 h after the reperfusion. The TUNEL-positive cells were significantly reduced by pretreatment with benidipine. The results demonstrate that benidipine can ameliorate the ischaemic acute renal failure in rats and suggest that the renoprotective effect of benidipine was at least partly attributable to the reduction of apoptosis in tubular epithelial cells.
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PMID:Benidipine inhibits apoptosis during ischaemic acute renal failure in rats. 1086 45

The objective of this investigation was to compare changes in antioxidant status (together with other metabolites relevant to hypertension) in plasma and cardiac tissue from spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY), following 8 weeks of treatment with lisinopril (angiotensin converting enzyme inhibitor) or amlodipine (Ca(2+) channel antagonist) respectively. There was no significant difference in the levels of total antioxidant capacity, retinol, urea, albumin or triglyceride in plasma from SHR or WKY rats, with or without lisinopril or amlodipine treatment. However in SHR rats, levels of alpha-tocopherol were substantially reduced in both plasma (-54% WKY, P<0.01) and cardiac tissue (-43% WKY, P<0.05). Treatment with lisinopril ameliorated reduced levels of plasma alpha-tocopherol in SHR rats, but not in cardiac tissue. Amlodipine treatment had no effect on alpha-tocopherol levels in plasma or cardiac tissue in SHR rats. In SHR rats total cholesterol levels were significantly lower thanWKY controls (-36%, P<0.001). This effect was reversed in lisinopril treated SHR rats (+27%, P<0.01). Plasma high density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol were reduced in untreated SHR rats (P<0.025) when compared to WKY controls; neither lisinopril nor amlodipine treatment significantly altered these parameters. These findings suggest possible alternative mechanisms of action for lisinopril, and reinforce its use in hypertensive patients or patients with left ventricular hypertrophy.
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PMID:Effects of lisinopril and amlodipine on antioxidant status in experimental hypertension. 1090 Feb 88

This paper examines the effect of enalapril in African-American (AA) females with advanced type 2 diabetic nephropathy (DN)--the leading cause of end stage renal disease (ESRD) in this group. AA females followed in our university nephrology clinic with type 2 DN and a serum creatinine level (Cr) > or = 2.5 mg/dl were eligible. Historical controls who never received an ACE inhibitor were selected (matched for age and Cr) from a database of patients reaching ESRD between 1993 and 1998, with a primary diagnosis of DN. Patients enrolled (N = 6) were started on enalapril at 5 mg per day with the dose titrated upward to a blood pressure (BP) goal of 140/90 mm Hg. The enalapril group tended to be older than controls (58.8 vs 51.5 years of age, P = ns) and had had their diabetes longer (18.5 vs 13.2 years of age, P = ns). At baseline, there were no significant differences in blood pressure, blood, urea, nitrogen (BUN), Cr, or BMI between groups. One of the 6 treated with enalapril had the agent stopped due to hyperkalemia. Five of 6 in the enalapril group reached ESRD, but there was no significant difference between the groups in the time it took to reach this stage (69.5 +/- 13.8 weeks vs 92.0 +/- 21.4 weeks, enalapril group vs control group, P = ns). In the enalapril patient who did not reach ESRD, the Cr level increased from 2.9 to 3.8 mg/dl in approximately 3 years. From this small study, we conclude that, although enalapril is tolerated in AA females with advanced DN, the agent had no significant effect on renal survival.
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PMID:The effect of enalapril on advanced diabetic nephropathy in African-American females. 1145 95

Intracranial aneurysms (ICA) are a well-known feature of autosomal dominant polycystic kidney disease. There is only one report about ICA in an adult patient with autosomal recessive polycystic kidney disease (ARPKD). We observed a 2-year, 6-month old girl with ARPKD and multiple ICA. The family history is negative for kidney disease. The diagnosis of ARPKD was based on the typical findings in ultrasonography and computed tomography. Cystic ectasia of biliary ducts 6.3/4.8 cm in diameter was found in the liver. Arterial hypertension in a range of 140/100-170/120 mm Hg was registered. The child has polyuria, polydipsia and enuresis. Blood urea was 15 mmol/l, creatinine in a range of 120 to 75 micromol/l. One episode of vomiting, dizziness and lethargy was the reason for a brain magnetic resonance imaging. Multiple fusiform and saccular aneurysms in the branches of middle and posterior cerebral arteries were seen bilaterally. The girl is growing well without neurological symptoms during an observation period of 1.5 years. Blood pressure is well controlled with an ACE inhibitor (Enalapril 2.5 mg daily). It was concluded that ICA can be found in patients with ARPKD. Blood pressure control is essential to reduce the risk of intracranial hemorrhage.
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PMID:Intracranial aneurysms in a child with autosomal recessive polycystic kidney disease. 1179 94

In recent years, it has been demonstrated that losartan lowers macroproteinuria in diabetic or non-diabetic renal transplant recipients (RTx) similar to angiotensin converting enzyme (ACE) inhibitors. Microalbuminuria (MAU) may reflect subclinical hyperfiltration damage of the glomerulus. It could be a marker of kidney dysfunction in renal transplantation. The aim of the study was to assess the efficacy of losartan in hypertensive RTx with MAU. This study was conducted in 17 (M/F: 4/13) stable RTx. No change was made in the medical treatment of the patients. All cases received 50 mg/day losartan therapy for 12 wk. Renal functions and MAU were determined 12 and 6 wk and just before the treatment as well as sixth and twelfth week of the treatment in all patients. Losartan satisfactorily lowered systemic blood pressure. A significant reduction in MAU was observed from 103 +/- 53 microg/min at the beginning to 59 +/- 25 microg/min in the sixth week and 47 +/- 24 microg/min in the twelfth week (p=0.0007 and 0.0005, respectively). From the sixth week of the treatment, the therapy significantly decreased hemoglobin, hematocrit and erythrocyte levels but did not change mean leukocyte and platelet counts, urea, creatinine levels and creatinine clearances. No serious side-effect was observed during the study. In conclusion, we found that losartan decreased MAU in hypertensive RTx. For that reason, it might be considered as the first choise antihypertensive agent for the renoprotection in selected patients.
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PMID:Angiotensin-II receptor antagonist losartan reduces microalbuminuria in hypertensive renal transplant recipients. 1201 Jan 44

BACKGROUND: Two separate cohorts of consecutive patients admitted to hospital with a primary diagnosis of heart failure were studied, the first in 1986 in Rochdale, and the second in 1995 in Brighton. METHODS: We observed the clinical profile, treatment and mortality during hospital admission and reviewed their status at 6 months. There were 132 patients in the Rochdale cohort and 223 in the Brighton cohort. RESULTS: The Rochdale cohort was characterised by a lower mean age and longer hospital stay. Significant differences were also observed in co-morbidity and the use of ACE inhibitors, but hospital mortality was almost identical (25% in Rochdale and 24% in Brighton). A low systolic blood pressure, hyponatraemia, hyperkalaemia and a raised blood urea at presentation were independent adverse prognostic factors. In contrast, prior treatment with ACE inhibitors in patients with congestive cardiac failure led to a more favourable hospital outcome. Age, gender and co-morbidity did not affect mortality apart from patients with acute myocardial infarction. Follow-up of these cohorts showed that mortality of the two groups remained high at 180 days after admission (40% in Rochdale and 39% in Brighton). There were marked differences in the use of ACE inhibitors in survivors, but target doses of ACE inhibitors (enalapril 20 mg/day or equivalent) were only achieved in 31%, despite direct communication between the hospital and primary care physicians. CONCLUSIONS: Although clinical and treatment profiles differed between the two periods studied, the hospital and 6-month mortality of patients with heart failure remained high. More emphasis needs to be given to optimising ACE inhibitor use in primary care.
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PMID:Heart failure in patients admitted to hospital: mortality is still high. 1214 9

OBJECTIVES. The present study was undertaken to determine if direct blockade of angiotensin II receptors by losartan potassium as compared to ACE inhibition might result in greater tolerability in patients with congestive heart failure in whom ACE inhibition resulted in hyperkalemia and azotemia. BACKGROUND. Blockade of angiotensin II receptors by losartan potassium may produce similar benefits in congestive heart failure as ACE inhibition. However, some observations suggest losartan potassium may have different effects on renal function than ACE inhibition. METHODS. Five consecutive patients with severe congestive heart failure were identified in whom treatment with ACE inhibition was complicated by hyperkalemia (K>5.7) and azotemia. In three of these patients losartan potassium was substituted for ACE inhibition while losartan potassium was added to treatment with ACE inhibition in the remaining two. The mean of four serial values of potassium, blood urea nitrogen, and creatinine were compared before and after change in treatment using a two-tailed t test. RESULTS. The addition or substitution of losartan potassium resulted in statistically insignificant reductions in blood urea nitrogen and creatinine and a significant reduction in potassium from 5.7+/-0.1 to 4.9+/-0.3, p<0.03. Two patients who had required kayexalate were withdrawn. In all patients, hyperkalemia resolved and did not reoccur. CONCLUSIONS. There appear to be fundamental differences between the effects of losartan potassium and ACE inhibitors on potassium excretion in congestive heart failure patients with mild to moderate renal insufficiency. Losartan potassium may also be associated with less azotemia in such patients. These differences may have important clinical implications, particularly in the subset of patients in whom ACE inhibition is poorly tolerated as a result of hyperkalemia and azotemia. (c)2000 by CHF, Inc.
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PMID:Differential effects of direct antagonism of AII compared to ACE inhibitors on serum potassium levels and azotemia in patients with severe congestive heart failure. 1214 52

Chronic renal failure (CRF) is almost always associated with high arterial blood pressure. Adequate control of hypertension slows down the progression of the disease, Inhibitors of angiotenzin-converting enzyme (ACE inhibitors) have proved to be very efficacious in decreasing high blood pressure. The aim of this study was to assess the influence of ACE inhibitor enalapril on the progression of CRF in patients with diabetic nephropathy and nephropathies of other origin. During 1998 and 1999 thirty patients (20 males and 10 females, aged 525 +/- 1.3) have been followed-up at the Department of Nephrology, Clinical Centre of Serbia. On regular monthly controls serum creatinine, urea, calcium and protein levels, creatinine clearance, and blood pressure, were measured. All patients were suggested a low protein diet. Progression of the disease was expressed by the slope of the regression line showing reciprocal serum creatinine values. Proteinaemia was significantly higher in diabetic patients after 12 months (p < 0.35), but in the next 12 months the difference between groups disappeared. The same patients had significantly lower serum urea (p < 0.05) after 24 months and creatinine values (p < 0.05) during the whole study. Other variables changed in the same manner and with similar progression in both groups. The direction of slope lines suggested recovery of kidney function in both examined groups. However, a smaller slope in patients with diabetic nephropathy together with other results showed that enalapril had better influence on slowing down the progression of CRF in this group of patients.
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PMID:[Effect of enalapril on progression of chronic renal insufficiency caused by diabetes and other etiologies: a 2-year study]. 1215 20


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