The reno-protective role of AT1-receptor blockers

Ce, Mogensen

doi:10.1038/sj.jhh.1001440

Cited by 18 publications

(9 citation statements)

References 52 publications

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“…However, a study on imidapril found no increase in reninangiotensin-aldosterone system blockade when dosages from 2.5 to 10 mg were compared (22). It is possible that alternative approaches to renin-angiotensin-aldosterone system blockade may be required (24). Such approaches may include the combination of ACE-I agents with angiotensin II receptor blockers (24 -26) or the use of aldosterone blockade agents such as spironolactone (27,28).…”

Section: Discussionmentioning

confidence: 99%

Determinants of Progression from Microalbuminuria to Proteinuria in Patients Who Have Type 1 Diabetes and Are Treated with Angiotensin-Converting Enzyme Inhibitors

Ficociello¹,

Perkins²,

Silva³

et al. 2007

Clinical Journal of the American Society of Nephrology

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The aims of this study were to assess the frequency and determinants of (1) treatment with angiotensin-converting enzyme inhibitors (ACE-I) and (2) progression to proteinuria in the presence of ACE-I treatment in patients with type 1 diabetes and microalbuminuria. A clinic-based cohort study of patients with type 1 diabetes was begun in 1991. The patients who were included in this study (n ‫؍‬ 373) are the cohort members who received a diagnosis of microalbuminuria during a 2-yr baseline observation and were followed for 10 yr with frequent assessments of urinary albumin excretion and biennial examinations. Progression to proteinuria occurred when the median urinary albumin excretion during a 2-yr interval exceeded 299 g/min. During the decade-long study, the proportion of patients who had a history of microalbuminuria and were treated with ACE-I rose from 17 to 67%. Patients who started this treatment had (on average) higher BP, higher urinary albumin excretion, and longer diabetes duration than those who did not. Microalbuminuria often progressed to proteinuria (6.3/100 person-years) in those who were treated. Poor glycemic control and elevated serum cholesterol were the major determinants/predictors of this progression. Although treatment with ACE-I increased during the past decade, it was not completely effective, because microalbuminuria progressed to proteinuria in many treated patients. Poor glycemic control and elevated serum cholesterol were the major determinants/predictors for progression while on ACE-I treatment. The mechanisms that are responsible for the frequent failure of ACE-I to prevent progression of microalbuminuria to proteinuria in a clinical setting are not clear.

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Section: Discussionmentioning

confidence: 99%

Determinants of Progression from Microalbuminuria to Proteinuria in Patients Who Have Type 1 Diabetes and Are Treated with Angiotensin-Converting Enzyme Inhibitors

Ficociello¹,

Perkins²,

Silva³

et al. 2007

Clinical Journal of the American Society of Nephrology

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“…23,24 Studies in patients with type II diabetes, who are usually overweight, clearly indicate that ACE inhibitors and ANG II receptor antagonists slow progression of renal disease. 24,51 However, additional studies are needed in nondiabetic obese subjects to determine whether RAS blockers are more effective than other antihypertensive agents in reducing the risk of renal injury.…”

Section: Renin-angiotensin System Alters Renal Function and Increasesmentioning

confidence: 99%

The Kidney, Hypertension, and Obesity

2003

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Abstract-This paper provides a personal perspective of the role of abnormal renal-pressure natriuresis in the pathogenesis of hypertension. Direct support for a major role of renal-pressure natriuresis in long-term control of arterial pressure and sodium balance comes from studies demonstrating that (1) pressure natriuresis is impaired in all forms of chronic hypertension and (2) prevention of pressure natriuresis from operating, by servo-control of renal perfusion pressure, also prevents the maintenance of sodium balance hypertension. Although the precise mechanisms of impaired pressure natriuresis in essential hypertension have remained elusive, recent evidence suggests that obesity and overweight may play a major role. Obesity increases renal sodium reabsorption and impairs pressure natriuresis by activation of the renin-angiotensin and sympathetic nervous systems and by altered intrarenal physical forces. Chronic obesity also causes marked structural changes in the kidneys that eventually lead to a loss of nephron function, further increases in arterial pressure, and severe renal injury in some cases. Although there are many unanswered questions about the mechanisms of obesity hypertension and renal disease, this is one of the most promising areas for future research, especially in view of the growing, worldwide "epidemic" of obesity.

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“…In particular, the evidence that telmisartan has the same beneficial effect of vitamin C in improving the long-lasting effect of hyperglycemia, in our opinion, deserves attention. In fact, the effectiveness of a chronic long-term treatment with vitamin C is still an open debate (35), whereas telmisartan and other AT-1 receptor blockers are already widely used for the prevention of diabetes complications, particularly nephropathy (36). It seems reasonable to suggest that an AT-1 receptor blocker is a much better form of therapy than vitamin C because a recent study indicates that vitamin C intake increases mortality in postmenopausal women with type 2 diabetes (37).…”

Section: Ceriello and Associatesmentioning

confidence: 99%

Telmisartan Shows an Equivalent Effect of Vitamin C in Further Improving Endothelial Dysfunction After Glycemia Normalization in Type 1 Diabetes

Ceriello

Piconi²,

Esposito

et al. 2007

Diabetes Care

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OBJECTIVE -Long-lasting hyperglycemia in type 1 diabetic patients induces permanent alterations of endothelial function by increased oxidative stress, even when glycemia is normalized.RESEARCH DESIGN AND METHODS -In this study, 36 type 1 diabetic patients and 12 control subjects were enrolled. The diabetic patients were divided into three groups. The first group was treated for 24 h with insulin, achieving a near normalization of glycemia. After 12 h of this treatment, vitamin C was added for the remaining 12 h. The second group was treated for 24 h with vitamin C. After 12 h of this treatment, insulin was started, achieving a near normalization of glycemia for the remaining 12 h. The third group was treated for 24 h with both vitamin C and insulin, achieving near normalization of glycemia. The same protocols were performed after 1 month of telmisartan or placebo.RESULTS -Neither normalization of glycemia nor vitamin C treatment alone was able to normalize endothelial dysfunction or oxidative stress. Combining insulin and vitamin C normalized endothelial dysfunction and decreased oxidative stress to normal levels. Telmisartan significantly improved basal endothelial function and decreased nitrotyrosine plasma levels. In patients treated with telmisartan, a near normalization of both flow-mediated vasodilation and oxidative stress was achieved when glycemia was normalized, whereas adding vitamin C infusion did not show further effect on endothelial function or nitrotyrosine plasma levels.CONCLUSIONS -These data indicate that combining the normalization of glycemia with an antioxidant can normalize endothelial function in type 1 diabetic patients and that telmisartan works as an antioxidant like vitamin C. Diabetes Care 30:1694-1698, 2007A n increase in the incidence of macrovascular diseases in type 1 diabetes has long been recognized (1). The acceleration of macrovascular disease is partly due to the increased incidence of classical risk factors such as hypertension and dyslipidemia (2). However, recent evidence suggests that hyperglycemia also plays a significant role (3).The endothelium is a major organ involved in the development of cardiovascular disease (CVD), even in diabetes, and the presence of endothelial dysfunction has often been reported in diabetes and been found to be an independent predictor of future CVD (4).Several studies have shown that hyperglycemia induces endothelial dysfunction in both diabetic and nondiabetic subjects (5-7); however, in type 1 diabetic patients, endothelial dysfunction has been reported to be present, even when normoglycemia is achieved (8,9).Evidence indicates that hyperglycemia induces endothelial dysfunction through the generation of oxidative stress (10), which has been suggested to be the key player in the generation of both micro-and macrovascular diabetes complications (11). We have recently demonstrated that a near normalization of endothelial dysfunction can be achieved in type 1 diabetic patients by combining an optimal control of glycemia with the infusion of t...

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The reno-protective role of AT1-receptor blockers

Cited by 18 publications

References 52 publications

Determinants of Progression from Microalbuminuria to Proteinuria in Patients Who Have Type 1 Diabetes and Are Treated with Angiotensin-Converting Enzyme Inhibitors

Determinants of Progression from Microalbuminuria to Proteinuria in Patients Who Have Type 1 Diabetes and Are Treated with Angiotensin-Converting Enzyme Inhibitors

The Kidney, Hypertension, and Obesity

Telmisartan Shows an Equivalent Effect of Vitamin C in Further Improving Endothelial Dysfunction After Glycemia Normalization in Type 1 Diabetes

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