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)

Hypertension is one of the main risk factors of mortality for children on renal replacement therapy. It has also been recognised as one of the major risk factors for progression of renal failure. The aim of the study was to define the prevalence of hypertension in children with chronic renal failure, treated in a single centre, and to assess the efficacy of its diagnosis and management. Hypertension was present in 27% of 40 children before the onset of chronic renal failure, increasing to 57% with the development of CRF, and reaching 86% at onset of dialysis. Reflux nephropathy, hemolytic-uraemic syndrome and glomerular disease were most frequently associated with severe hypertension. ACE inhibitors (70%), diuretics (52%), and calcium channel blockers were the most frequently used antihypertensives with 49% of the children being on monotherapy. Despite therapy 43% of children had elevated blood pressure levels and 16% had echocardiographic signs of LVH. A 24 hour ambulatory blood pressure measurements were more sensitive in diagnosing hypertension and assessing adequacy of blood pressure control. Early and intensified treatment should prevent end organ damage though optimal blood pressure values to aim obtain are still to be defined.
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PMID:[Hypertension in children with chronic renal failure]. 1089 39

Hypertension is almost an inevitable complication of chronic renal failure and it contributes to the acceleration of its progression to terminal renal failure. Cohort studies and large scale clinical trials carried out in the last 10 years have allowed quantification of the respective influences and interactions of hypertension, proteinuria, and metabolic factors on the rate of degradation of renal function. They have conclusively showed a benefit in normalising the blood pressure in diabetic and nondiabetic renal disease especially when the proteinuria is pronounced and when the treatment includes an angiotensin converting enzyme inhibitor. Hypertension is also an increasingly common cause of renal failure, which may become terminal by its consequences associating vascular and ischaemic lesions of the renal parenchyma. Depending on the country studied, 10 to 25% of new dialysis patients are now classified as hypertensive and vascular renal disease. The individual renal risk of essential hypertension is relatively low except in certain groups, such as the coloured population, especially in the USA. The risk of a significant increase in creatinine is doubled by any increase of 20 mmHg of diastolic blood pressure but long-term studies suggest that the effects of increased systolic blood pressure may be even greater.
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PMID:[Hypertension and renal insufficiency]. 1119 Feb 96

Aggravation of anemia in chronic renal failure patients by angiotensin-converting enzyme inhibitors (ACEIs) has been attributed to the inhibition of angiotensin II which facilitates erythropoietin(Epo) production. This study was aimed at evaluating whether ACEIs aggravate anemia in maintenance hemodialysis patients and to investigate the influence of ACE gene polymorphism on erythropoiesis in these patients. Ninety-one hemodialysis patients were divided into 2 groups, based on whether or not they were administered ACEIs, into the ACEI group(n = 24) and the non-ACEI group(n = 67), and comparisons were made of the doses of recombinant human Epo(rHuEpo) administered, the hematocrit(Hct) and the plasma Epo concentrations. Among the patients in the non-ACEI group, only 17 did not receive rHuEpo, while all of the patients in the ACEI group received rHuEpo. The average dose of rHuEpo was 102.7 +/- 45.4 IU/kg/week in the ACEI group and 57.8 +/- 55 IU/kg/week in the non-ACEI group and the difference between the two groups was statistically significant. A statistically significant difference in the Hct was also observed between the two groups: the mean Hct in the ACEI group was 28.7 +/- 2.9% while that in the non-ACEI group was 31.1 +/- 3.7%. The plasma Epo concentrations were significantly lower in the ACEI group than in the non-ACEI group. No significant differences in the rHuEpo dose and Hct were observed between the three ACE genotype classes in either the ACEI or the non-ACEI group, however, there was a significant difference among the three genotypes in the non-ACEI group in regard to the plasma Epo concentrations; patients with the DD genotype had higher concentrations than those with the DI or II genotypes. These data suggest that anemia in maintenance hemodialysis patients is worsened by ACEIs as a result of the suppression of Epo production. Although it has been suggested that the endogenous Epo concentrations in maintenance hemodialysis patients are associated with ACE gene polymorphism, no significant influence of the ACE genotype on the rHuEpo dose or Hct was evident. Therefore, it is possible that exacerbation of anemia by ACEIs in the patients receiving rHuEpo is a result of an inhibited bone marrow response to Epo.
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PMID:[The effects of ACE inhibitor treatment and ACE gene polymorphism on erythropoiesis in chronic hemodialysis patients]. 1119 99

Losartan is the first of a new category of drug that inhibits angiotensin II (ANG II) AT1 receptors antagonists. This drug lowers blood pressure by inhibiting the activity of ANG II and reduces proteinuria and progression of chronic renal failure (CRF). It seems therefore an extremely interesting drug. Aim of this study is to describe 3 cases of acute renal failure (ARF), occurred during therapy with losartan. None of the patients showed renal arteries stenosis or other predisposing factors for the development of ARF. In conclusion, we want pointed out that losartan could affect renal function in a similar way as angiotensin converting enzyme inhibitors (ACEI). We suggested that use of losartan in risk situations, like old age, preexiting CRF, stenosis of renal arteries, solitary kidney and diuretic therapy, should be carefully monitored as well as that of ACE I.
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PMID:[Acute kidney failure and losartan: a recently observed event of antagonists of angiotensin II AT1 receptors]. 1122 61

In recent years, a target blood pressure (BP) of at least 125/75 mmHg has been sought in order to reduce the rate of progression of chronic renal failure (CRF) and cardiovascular mortality. Some antihypertensive agents, such as ACE inhibitors, calcium channel blockers and angiotensin receptor antagonists (and perhaps endothelin converting enzyme inhibitors and endothelin antagonists), may also reduce CRF progression because they block some of the pathogenetic mechanisms involved in renal damage. Although this effect seems to be partially independent of BP reduction, it is still not clear whether these drugs are really superior to other antihypertensive agents when low BP is achieved. However, the possibility that combination treatments with some of these drugs may confer additive or even synergistic renoprotective effects other than BP control is not only fascinating, but also important because multidrug antihypertensive regimens are required anyway to manage BP adequately in the majority of patients with CRF.
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PMID:The renoprotective effect of combined antihypertensive drugs. 1128 47

The development of pharmacological agents that block the renin-angiotensin system (RAS) specifically have helped to define all the components of the system and their contribution to blood-pressure control and to the pathogenesis of hypertension, congestive heart failure and chronic renal failure. The angiotensin converting-enzyme inhibitors (ACEi) are among all available drugs that interfere with the RAS, the most efficient, so far, in the treatment of several cardiovascular diseases, with comfortable posologic schemes and an acceptable safety profile. The most important difference between them are more related to pharmacokinetic profile rather than to pharmacodynamic characteristics. With the use of ACEi the interference with other neurohumoral systems is unavoidable and the controversy has been pharmacologically and clinically installed. With the advent of oral selective AT1 angiotensin II receptor blockers (ARB) the pharmacological interference became eventually much more selective. Their antihypertensive efficacy is identical and their tolerability is better than that showed by ACEi. The ARBs differ mainly in their pharmacokinetics and in their binding capacity to the AT1 angiotensin receptor. The results of several ongoing clinical trials will show if the ARBs as ACEi will be capable to protect target-organs and to promote a significant reduction in cardiovascular morbility and mortality. In parallel there is an intense experimental and clinical research with other groups of drugs which also markedly interfere with RAS: renin inhibitors, chymase inhibitors and simultaneous inhibitors of vasopeptidases (ACE, endothelin converting-enzyme, neutral endopeptidase). From the pharmacological point of view, it is now possible to block effectively RAS with some relevant clinical results that will be certainly widen in the near future.
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PMID:[Angiotensin converting enzyme inhibitors (ACEIs) and angiotensin II receptor antagonists. Pharmacologic features]. 1130 8

Atheromatous renovascular disease (ARVD) is a common cause of hypertension and chronic renal failure (CRF). In this unit, intravenous digital subtraction angiography (DSA) (or intraarterial DSA if indicated) is used as a screening angiographic study when ARVD is suspected. However, increased use of these investigations has resulted in a longer waiting time for angiography. As the majority of studies are negative for ARVD, clinical features and results of investigations of patients undergoing angiography were reviewed to identify those having the greatest likelihood of ARVD. The clinical notes were reviewed for all 249 patients undergoing angiography over an 18-month period. Primary indications for investigation were: hypertension 71 (28.5%), CRF 156 (62.7%) and CRF with severe hypertension 22 (8.8%). 12 of the CRF patients had end-stage renal failure. 166 (66.7%) patients had no evidence of ARVD, while only 83 (33.3%) patients showed some degree of ARVD, 29 (35%) of which had bilateral renal artery disease. There was no significant difference between the ARVD group and the non-ARVD group for mean age (69.0 years vs 63.3 years), male to female ratio, history of smoking (68.7% vs 55.4%), severe hypertension (10.8% vs 9.0%), hypercholesterolaemia (61.4% vs 47.0%), diabetes mellitus (28.6% vs 25.3%) or angiotensin converting enzyme inhibitor-related renal dysfunction (9.6% vs 6.1%). More patients in the ARVD group were investigated for CRF than in the non-ARVD group, as reflected by the higher serum creatinine level and the lower creatinine clearance in the ARVD group. 55 (33.1%) of the non-ARVD patients had no comorbid vascular disease, vascular bruits or ultrasound discrepancy in the size of the two kidneys, whereas all ARVD patients had at least one of these features (negative predictive value 100%). All three features were present in 19.3% of ARVD patients but in only 3.0% of the non-ARVD patients (positive predictive value 76.2%, specificity 97%). We plan to rationalize the criteria for angiography in the light of these findings, anticipating an increase in the diagnostic yield of renal angiography from its current 33.3% to above 42%.
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PMID:Increasing the diagnostic yield of renal angiography for the diagnosis of atheromatous renovascular disease. 1133 95

The number of patients who needs for dialysis therapy is increasing rapidly among the older population. Although control of hypertension can delay or arrest the progression of renal failure, there are lacking of studies about antihypertensive treatment of chronic renal failure in the elderly. We have studied the effects of treating hypertension with a calcium antagonist, benidipine, on renal function and blood pressure in 58 patients (mean age: 71 +/- 9) with hypertension and chronic renal insufficiency (the levels of creatinine ranging from 1.5 to 4.0 mg/dl). The underlying disease included glomerulopathies (in 33), diabetic nephropathy (in 15), and other causes (in 10). Forty two patients who had been treated with other antihypertensive drugs other than angiotensin converting enzyme (ACE) inhibitors, antihypertensive drugs were withdrawn 2 weeks before the entry. At the entry, patients should have sitting systolic blood pressure (SBP) of above 160 mmHg and diastolic blood pressure (DBP) of above 90 mmHg. In total, both SBP and DBP decreased from 169/95+/-12.5/8.9 to 148/81+/-16.1/8.0 mmHg (p<0.001) with remaining the serum creatinine levels from 2.2+/-0.8 vs 2.4+/-1.3 mg/dl (P>0.05). Retrospective analysis revealed that in 4 of 4 patients treated with benidipine and 2 of 3 patients with benidipine and ACE inhibitors with systolic blood pressure more than 160 mmHg at the end of the study, the levels of serum creatinine increased from 2.5+/-0.3 to 2.8+/-0.4 with significance (P<0.05). If systolic blood pressure was reduced less than 159 mmHg, 38 of 48 patients did not show any deterioration of renal function. Compared to the significance of SBP in preserving renal function, DBP did not associate with the changes in renal function. No patients died during the study. One patient had transient ischemic attack and one patient had stroke in benidipine treated group. One patient had angina pectoris in benidipine-ACE inhibitors treated group. The results of our trial seem to give some support for the idea that long-acting calcium antagonists such as benidipine are renoprotective through reduction of SBP in the elderly people with hypertension and chronic renal insufficiency. However, if systolic blood pressure was not reduced below 160 mmHg throughout a year, the substantial declines in renal function would be expected.
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PMID:Effects of calcium antagonist, benidipine, on the progression of chronic renal failure in the elderly: a 1-year follow-up. 1133 86

To investigate the role of the angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism on prevalence and progression of disease in children with chronic renal failure (CRF), we determined the ACE I/D genotype in 95 children with CRF due to renal malformations (hypo-/dysplasia, obstructive uropathy, reflux nephropathy; n = 59), other congenital or hereditary diseases (n = 23), or acquired glomerular disorders (n = 13), who had been followed prospectively over a 2-year period. CRF progression rate was followed in each individual by linear regression analysis of estimates of glomerular filtration rate (GFR) obtained every 2 months. Actuarial renal 'survival' analysis was performed, using a GFR loss of 10 ml/min per 1.73 m2 as a cutoff point. The distribution of the ACE genotype did not differ among the disease groups. There was also no difference in ACE genotype distribution between the patients and a control group of healthy Caucasian children (n = 163). Among the children with renal malformations, the 2-year renal survival was significantly lower in those with the DD genotype (61%) than in patients with ID or II genotype (89%, P < 0.01). In the other disease groups, the ACE I/D genotype was not predictive of CRF progression. In a multivariate analysis of risk factors, the adverse effect of the DD genotype (risk ratio 10.2, P < 0.05) was independent of and additive to those of arterial hypertension (RR 13.2, P < 0.001) and gross proteinuria (RR 4.7, P < 0.05). We conclude that the ACE DD genotype is a significant risk factor for children with congenital renal malformations to develop progressive CRF. The effect of the ACE polymorphism in this patient group is independent of hypertension and proteinuria.
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PMID:Impact of ACE I/D gene polymorphism on congenital renal malformations. 1135 81

Chronic renal failure (CRF) is a complex phenotype, which results from the underlying kidney disease and superimposing environmental and genetic factors. The aim of the study was to evaluate the role of angiotensin converting enzyme gene Pst 1 polymorphism in the development and/or progression of CRF. 247 family trios (patients with CRF and both parents): 120 with primary chronic glomerulonephritis, 80 with interstitial nephritis and 47 with diabetic nephropathy were examined, and transmission/disequilibrium test (TDT) was used to evaluate allele transmission from heterozygous parents to affected off-spring. No significant deviation from random transmission of the examined ACE gene Pst 1 alleles was observed, as well as no impact of this marker on the rate of progression of chronic renal failure.
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PMID:[The role of angiotensin I converting enzyme (ACE) Pst 1 polymorphism in the development of chronic renal failure]. 1139 61


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