UMLS:C0730345 - FACTA Search

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Query: UMLS:C0730345 (microalbuminuria)
4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the study was to compare the effect of treatment with an angiotensin converting enzyme inhibitor (Lisinopril, MSD) or calcium blocker (Nifedipine retard, MSD) treatment during three months on blood pressure (measured with sphygmomanometric method and ambulatory blood pressure monitoring--ABPM) and urinary albumin excretion in essential hypertension class I acc. to WHO. Fifteen untreated patients aged 38 +/- 5 years with essential hypertension participated in the study and received diet with normal sodium content. Urinary albumin excretion was measured by RIA method in two 24 hour urine collections and mean value was calculated. ABPM was measured with Spacelabs monitor. After first examination 8 patients were randomly selected for the treatment with lisinopril and 7 patients to the treatment with nifedipine. The doses of both drugs were gradually adjusted to reach diastolic blood pressure below 90 mmHg. After 3 months of treatment urinary albumin excretion and blood pressure was found in both after treatment in patients treated with lisinopril but not in those receiving nifedipine. In patients treated with lisinopril a correlation between the decrease in systolic and diastolic blood pressure (measured by ABPM) and decrease of urinary albumin excretion was demonstrated. It was concluded that the normalization of blood pressure induced by lisinopril treatment in patients with uncomplicated essential hypertension and normoalbuminuria is accompanied with significant diminution of urinary albumin excretion which suggests preventive action of the drug in the development of microalbuminuria. Diminution of urinary albumin excretion caused by lisinopril is probably due to both the decrease of blood pressure and the specific renal action of the drug.
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PMID:[Comparison of treatment effects with an angiotensin converting enzyme inhibitor--lisinopril and a calcium blocker--nifedipine retard on urinary albumin excretion in patients with non-complicated essential hypertension]. 747 31

Lisinopril, like other ACE inhibitors, lowers blood pressure and preserves renal function in hypertensive patients with non-insulin-dependent or insulin-dependent diabetes mellitus (NIDDM or IDDM) and early or overt nephropathy, without adversely affecting glycaemic control or lipid profiles. On available evidence, renoprotective effects appear to be greater with lisinopril than with comparator calcium channel blockers, diuretics and beta-blockers, despite similar antihypertensive efficacy. As shown by the EUCLID (EUrodiab Controlled trial of Lisinopril in Insulin-Dependent Diabetes) trial, lisinopril is also renoprotective in normotensive patients with IDDM and microalbuminuria. The effect in normotensive patients with normoalbuminuria was smaller than in those with microalbuminuria, and no conclusions can yet be made about its use in patients with normoalbuminuria. In complications other than nephropathy, lisinopril has shown some benefit. Progression to retinopathy was slowed during 2 years' lisinopril therapy in the EUCLID study. Although not yet fully published, these results provide the most convincing evidence to date for an effect of an ACE inhibitor in retinopathy. The drug may also improve neurological function, but this finding is preliminary. Lastly, post hoc analysis of the GISSI-3 trial indicates that lisinopril reduces 6-week mortality rates in diabetic patients when begun as early treatment after an acute myocardial infarction. The tolerability profile of lisinopril is typical of ACE inhibitors and appears to be similar in diabetic and nondiabetic individuals. Hypoglycaemia has occurred at a similar frequency with lisinopril and placebo, as shown in the EUCLID trial. In addition, the GISSI-3 study indicates that the incidence of persistent hypotension and renal dysfunction is increased with lisinopril in general, but the presence of diabetes does not appear to confer additional risk of these events in diabetic patients with acute myocardial infarction receiving lisinopril. In summary, lisinopril lowers blood pressure and produces a renoprotective effect in patients with IDDM and NIDDM without detriment to glycaemic control or lipid profiles. Like other ACE inhibitors, lisinopril should thus be viewed as a first-line agent for reducing blood pressure and preventing or attenuating nephropathy in hypertensive diabetic patients with IDDM or NIDDM and microalbuminuria or overt renal disease. The EUCLID study, using lisinopril, provides new data supporting an additional place in managing normotensive patients with microalbuminuria and IDDM. These findings, together with some evidence for an effect of lisinopril in delaying progression of retinopathy and in reducing mortality, suggest a broader role for the drug in managing diabetic vascular complications.
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PMID:Lisinopril. A review of its pharmacology and use in the management of the complications of diabetes mellitus. 917 32

Recent studies have further elucidated the association between blood pressure and albumin excretion in insulin-dependent diabetes mellitus (IDDM) patients with (i) normal urinary albumin excretion (UAE), and (ii) moderate microalbuminuria (20 to 70 micrograms/min). In a study comprising 117 normoalbuminuric (UAE < 20 micrograms/min) patients we performed 24-hour ambulatory blood pressure monitoring (AMBP), and short-term power spectral analysis of RR interval oscillations. In comparison with the group with a UAE below the median, patients with UAE above the median were characterized by: significantly higher 24-hour systolic and diastolic AMBP, significantly reduced short-term RR interval variability, and significantly higher HbA1c. In a double blind study, normotensive IDDM patients with moderate microalbuminuria (20 to 70 micrograms/min) were randomized to either lisinopril (20 mg once a day, N = 12) or placebo (N = 10) for two years. In the lisinopril group there were significant reductions in 24-hour systolic and diastolic AMBP compared to the placebo group. Lisinopril did not attenuate the diurnal blood pressure variation. UAE tended to be reduced in the lisinopril group. A significantly positive association between changes in AMBP and changes in UAE was present in the placebo group in contrast to the lisinopril group. Changes in UAE were strongly and positively associated with changes in filtration fraction in the lisinopril treated group. In conclusion, interactions between albumin excretion, blood pressure, autonomic function, and glycemic status are already detectable within the normoalbuminuric range in IDDM patients. Angiotensin converting enzyme inhibitor (ACEi) treatment in a small group of normotensive IDDM patients with moderate microalbuminuria reduces blood pressure without attenuating diurnal blood pressure variation, tends to reduce albumin excretion, and abolishes the association between changes in UAE and changes in blood pressure observed in the placebo group. ACEi intervention in selected normoalbuminuric high risk patients (high-normal UAE, high-normal blood pressure, and poor glycemic control) would be of interest.
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PMID:High normo- or low microalbuminuria: basis for intervention in insulin-dependent diabetes mellitus. 940 13

We examined whether the ACE gene insertion/deletion (I/D) polymorphism modulates renal disease progression in IDDM and how ACE inhibitors influence this relationship. The EURODIAB Controlled Trial of Lisinopril in IDDM is a multicenter randomized placebo-controlled trial in 530 nonhypertensive, mainly normoalbuminuric IDDM patients aged 20-59 years. Albumin excretion rate (AER) was measured every 6 months for 2 years. Genotype distribution was 15% II, 58% ID, and 27% DD. Between genotypes, there were no differences in baseline characteristics or in changes in blood pressure and glycemic control throughout the trial. There was a significant interaction between the II and DD genotype groups and treatment on change in AER (P = 0.05). Patients with the II genotype showed the fastest rate of AER progression on placebo but had an enhanced response to lisinopril. AER at 2 years (adjusted for baseline AER) was 51.3% lower on lisinopril than placebo in the II genotype patients (95% CI, 15.7 to 71.8; P = 0.01), 14.8% in the ID group (-7.8 to 32.7; P = 0.2), and 7.7% in the DD group (-36.6 to 37.6; P = 0.7). Absolute differences in AER between placebo and lisinopril at 2 years were 8.1, 1.7, and 0.8 microg/min in the II, ID, and DD groups, respectively. The significant beneficial effect of lisinopril on AER in the II group persisted when adjusted for center, blood pressure, and glycemic control, and also for diastolic blood pressure at 1 month into the study. Progression from normoalbuminuria to microalbuminuria (lisinopril versus placebo) was 0.27 (0.03-2.26; P = 0.2) in the II group, and 1.30 (0.33-5.17; P = 0.7) in the DD group (P = 0.6 for interaction). Knowledge of ACE genotype may be of value in determining the likely impact of ACE inhibitor treatment.
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PMID:Effect of angiotensin-converting enzyme (ACE) gene polymorphism on progression of renal disease and the influence of ACE inhibition in IDDM patients: findings from the EUCLID Randomized Controlled Trial. EURODIAB Controlled Trial of Lisinopril in IDDM. 972 42

SURROGATE END-POINTS FOR PROGNOSIS OF HYPERTENSION: The identification of surrogate measures of cardiovascular risk in patients with hypertension may allow clinicians to better estimate a patient's long-term prognosis and monitor the effects of antihypertensive therapy in reducing risk and thereby reducing the cardiovascular complications of hypertension. PROGNOSTIC LIMITATIONS OF OFFICE BLOOD PRESSURE: Previous studies have shown that office blood pressure may predict the incidence of fatal and nonfatal cardiovascular complications of hypertension. However, evidence also suggests that the predictive value of office blood pressure is limited and that it does not provide accurate estimates of the changes in the cardiovascular risk profile that can occur with antihypertensive treatment. PROGNOSTIC VALUE OF 24-H AMBULATORY BLOOD PRESSURE: Cross-sectional studies have shown that 24-h average blood pressure values are more closely correlated with hypertensive target-organ damage [e.g. left ventricular hypertrophy (LVH), retinopathy, increased serum creatinine, albuminuria, and microalbuminuria] than are office blood pressure values. Although longitudinal evidence of the clinical relevance of 24-h ambulatory blood pressure monitoring is limited, preliminary data from a recently completed trial, the Study on Ambulatory Pressure and Lisinopril Evaluation (SAMPLE), have clearly shown the superiority of 24-h blood pressure monitoring over office readings in predicting the regression of LVH in hypertensive patients following treatment to reduce blood pressure.
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PMID:Can good surrogate end-points predict the prognosis of hypertensive patients? 986 98

The main objective of the CALM (Candesartan And Lisinopril Microalbuminuria) study is to assess the effect of a dual blockade of the renin-angiotensin system--using both an angiotensin converting enzyme inhibitor (ACE-I) and an angiotensin II type 1 receptor blocker--in patients with type 2 diabetes, high blood pressure and microalbuminuria. The study included 200 patients randomized to receive candesartan 16 mg or lisinopril 20 mg for 12 weeks, followed by 12 weeks of the same monotherapy or a combination treatment. Main outcomes are the reduction of microalbuminuria and blood pressure. All three of the treatments are effective, but the dual blockade is respectively 18%, 8 mmHg and 5 mmHg more effective in reducing microalbuminuria, systolic and diastolic blood pressure. No comparison is made between this "new" association and the more frequently used biotherapy (i.e. ACE-I plus thiazidic diuretic) and therefore its usefulness in regular practice is still to be determined.
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PMID:[Clinical study of the month. The CALM study assessing the combination of an angiotensin-converting enzyme inhibitor and an angiotensin II receptor antagonist in the treatment of diabetic nephropathy]. 1129 48

Although current hypertension management guidelines recommend increasingly stringent blood pressure targets, these targets are seldom achieved in clinical practice. Even in patients with mild-to-moderate hypertension, monotherapy is only effective in approximately 50-70% of patients, and thus there is a clear need for combination therapy if stringent blood pressure targets are to be achieved. Drugs used in combination therapy should satisfy a number of prerequisites, including complementary mechanisms of action, enhanced efficacy in combination, and maintained (or improved) tolerability. Evidence is accumulating that combination therapy with an AT(1)-receptor blocker and a diuretic represents a rational and effective treatment option. In clinical trials, the combination of candesartan cilexetil, 16 mg, and hydrochlorothiazide, 12.5 mg, has been shown to be more effective in lowering blood pressure than either agent alone. Furthermore, this combination has been shown to reduce blood pressure to a greater extent, and control blood pressure in a higher proportion of patients, than the combination of losartan, 50 mg, and hydrochlorothiazide, 12.5 mg, both when used instead of or in addition to previous antihypertensive therapy. The placebo-like tolerability of AT(1)-receptor blockers was maintained when these drugs were used in combination with hydrochlorothiazide. The combination of candesartan and a dihydropyridine calcium antagonist has also been shown to be more effective than either component alone. Furthermore, in the Candesartan and Lisinopril Microalbuminuria (CALM) Study, the combination of candesartan and lisinopril reduced blood pressure to a greater extent than either agent alone, and tended to have a greater effect on microalbuminuria.
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PMID:Combination therapy with AT(1)-receptor blockers. 1214 Jul 24

Diabetes mellitus increases the risk for hypertension and associated cardiovascular diseases, including coronary, cerebrovascular, renal and peripheral vascular disease. The risk for developing cardiovascular disease is increased when both diabetes and hypertension co-exist; in fact, over 11 million Americans have both diabetes and hypertension. These numbers will continue to climb, internationally, since the leading associated risk for diabetes development, obesity, has reached epidemic proportions, globally. Moreover, the frequent association of diabetes with dyslipidemia, as well as coagulation, endothelial, and metabolic abnormalities also aggravates the underlying vascular disease process in patients who possess these comorbid conditions. The renin-angiotensin-aldosterone system (RAS) and arginine vasopressin (AVP) are overactivated in both hypertension and diabetes. Drugs that inhibit this system, such as ACE inhibitors and more recently angiotensin receptor antagonists (ARBs), have proven beneficial effects on the micro- and macrovascular complications of diabetes, especially the kidney. The BRILLIANT study showed that lisinopril reduces microalbuminuria better than CCB therapy. Numerous other long-term studies confirm this association with ACE inhibitors including the HOPE trial. Furthermore, the European Controlled trial of Lisinopril in Insulin-dependent Diabetes (EUCLID) study, showed that lisinopril slowed the progression of renal disease, even in individuals with mild albuminuria. In fact, there are now five appropriately powered randomized placebo-controlled trials to show that both ACE inhibitors and ARBs slow progression of diabetic nephropathy in people with type 2 diabetes. These effects were shown to be better than conventional blood pressure lowering therapy, including dihydropyridine CCBs. In patients with microalbuminuria, ACE inhibitors and ARBs reduce the progression of microalbuminuria to proteinuria and provide a risk reduction of between 38 and 60% for progression to proteinuria. This is important since microalbuminuria is known to be associated with increased vascular permeability and decreased responsiveness to vasodilatory stimuli. Recently, increased AVP levels have been lined to microalbuminuria and hyperfiltration in diabetes. The microvascular and macrovascular benefits of ACE inhibition, ARBs and possible role of AVP antagonists in diabetic patients will be discussed, as will be recommendations for its clinical use.
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PMID:Treatment of the diabetic patient: focus on cardiovascular and renal risk reduction. 1243 44

Angiotensin-converting enzyme (ACE) inhibitors have favourable effects on hypertension and diabetic nephropathy, but persistent use may result in incomplete blockade of the renin-angiotensin system. Long-term effects of dual blockade using the ACE inhibitor lisinopril and the long-acting angiotensin II receptor blocker (ARB) telmisartan on blood pressure and albumin excretion rate (AER) were evaluated. Patients with type 2 diabetes mellitus, hypertension (systolic blood pressure [SBP] >or=140 mmHg or diastolic blood pressure [DBP] >or=90 mmHg) and microalbuminuria (AER 30-300 mg/24h) received 20mg of lisinopril or 80 mg of telmisartan once a day for 24 weeks. Patients were then randomised to continuing treatment with the respective monotherapy or with lisinopril plus telmisartan for a further 28 weeks. Significant (P<0.001) declines in SBP (11.1 mmHg versus 10.0 mmHg), DBP (5.6 mmHg versus 5.3 mmHg) and AER (98 mg/24 h versus 80 mg/24 h) were achieved with lisinopril (n=95) or telmisartan (n=97), respectively, after 24 weeks. Subsequent treatment with lisinopril plus telmisartan for 28 weeks resulted in further significant reductions (P<0.001) in SBP, DBP and AER compared with either monotherapy. All treatments were well tolerated. Lisinopril plus telmisartan thus provides superior blood pressure and AER control than either monotherapy. We conclude that use of dual blockade may provide a new approach to prevention of diabetic nephropathy in patients with type 2 diabetes, hypertension and microalbuminuria.
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PMID:Beneficial effect of lisinopril plus telmisartan in patients with type 2 diabetes, microalbuminuria and hypertension. 1611 44

Decreased left ventricular long-axis function may be the earliest stage in subclinical heart failure in Type II diabetes. To assess whether a decrease in SBP (systolic blood pressure) or a change in metabolic control would improve the long-axis function, 48 Type II diabetic patients participating in the CALM II (Candesartan and Lisinopril Microalbuminuria II) study were included in the present study. Patients were examined with tissue Doppler echocardiography at baseline and after 3 and 12 months of follow-up. Corresponding blood pressure, fructosamine and HbA(1c) (glycated haemoglobin) values were obtained. During the follow-up period, a decrease in SBP of 8 mmHg was seen (from 141+/-11 mmHg at baseline to 133+/-12 mmHg; P<0.001) and the peak systolic strain rate was significantly improved (from -1.10+/-0.25 at baseline to -1.25+/-0.22; P<0.01). There was a highly significant relationship between the changes in systolic strain rate, HbA(1c) (P<0.001) and fructosamine (P<0.05), and similarly to changes in left ventricular mass (P<0.05), whereas the correlation to the SBP reduction was not significant. Patients with improved glycaemic control, defined as a reduced HbA(1c) value after 12 months of follow-up, had a significantly improved strain rate (from -1.07+/-0.3 s(-1) at baseline to -1.32+/-0.25 s(-1); P<0.01) compared with patients with increases in HbA(1c) (from -1.14+/-0.25 s(-1) at baseline to -1.16+/-0.27 s(-1); P=not significant). The two groups had comparable baseline values of SBP, left ventricular mass, age and disease duration. In conclusion, changes in left ventricular systolic long-axis function are significantly correlated with changes in left ventricular mass, as well as metabolic control, in hypertensive patients with Type II diabetes mellitus.
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PMID:Effects of blood pressure lowering and metabolic control on systolic left ventricular function in Type II diabetes mellitus. 1651 87

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