Long-term comparison between perindopril and nifedipine in normotensive patients with type 1 diabetes and microalbuminuria

Jerums, George; Allen, Terri J.; Campbell, Duncan J.; Cooper, Mark E.; Gilbert, Richard E.; Hammond, Jeremy; Raffaele, J F; Tsalamandris, Con

doi:10.1016/s0272-6386(05)80003-4

Cited by 70 publications

(47 citation statements)

References 34 publications

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“…As has been described previously (18), perindopril provides superior protection from declining renal disease as compared with nifedipine for equivalent BP lowering. Plasma taken from patients with type 1 diabetes in the placebo group had significantly higher LMW-AGE concentrations at the completion of the study period than did patients who were treated with the ACEi perindopril (Figure 6A).…”

Section: Increases In Circulating Age Levels Are Accompanied By Decrementioning

confidence: 62%

“…The criteria for inclusion were patients who were aged 16 to 65 yr and had a duration of type 1 diabetes for Ͼ5 yr. All patients had microalbuminuria, diagnosed on three separate occasions (AER 20 to 200 g/min) and supine BP of Ͻ160/90 mmHg if older than 40 yr of age or 140/90 if younger than 40 yr (18). The exclusion criteria were nondiabetic renal disease, evidence of poor diabetic control (HbA 1c Ͼ10%), cardiac failure, and systemic disease (18). All human procedures were in accordance with guidelines set by the Austin Hospital Human Ethics Committee and the National Health and Medical Research Council of Australia.…”

Section: Human Plasma Samplesmentioning

confidence: 99%

“…This was investigated in a series of studies that included a cell culture model and a long-term model of exper-imental diabetic nephropathy and in samples from patients who had type 1 diabetes and participated in a clinical trial that explored early renoprotection with the ACEi perindopril (18).…”

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confidence: 99%

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Modulation of Soluble Receptor for Advanced Glycation End Products by Angiotensin-Converting Enzyme-1 Inhibition in Diabetic Nephropathy

Forbes¹,

Thorpe²,

Thallas‐Bonke³

et al. 2005

Journal of the American Society of Nephrology

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196

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Recent studies have identified that first-line renoprotective agents that interrupt the renin-angiotensin system not only reduce BP but also can attenuate advanced glycation end product (AGE) accumulation. This study used in vitro, preclinical, and human approaches to explore the potential effects of these agents on the modulation of the receptor for AGE (RAGE). Bovine aortic endothelial cells that were exposed to the angiotensin-converting enzyme inhibitor (ACEi) ramiprilat in the presence of high glucose demonstrated a significant increase in soluble RAGE (sRAGE) secreted into the medium. In streptozotocininduced diabetic rats, ramipril treatment (ACEi) at 3 mg/L for 24 wk reduced the accumulation of skin collagen-linked carboxymethyllysine and pentosidine, as well as circulating and renal AGE. Renal gene upregulation of total RAGE (all three splice variants) was observed in ACEi-treated animals. There was a specific increase in the gene expression of the splice variant C-truncated RAGE (sRAGE). There were also increases in sRAGE protein identified within renal cells with ACEi treatment, which showed AGE-binding ability. This was associated with decreases in renal full-length RAGE protein from ACEi-treated rats. Decreases in plasma soluble RAGE that were significantly increased by ACEi treatment were also identified in diabetic rats. Similarly, there was a significant increase in plasma sRAGE in patients who had type 1 diabetes and were treated with the ACEi perindopril. Complexes between sRAGE and carboxymethyllysine were identified in human and rodent diabetic plasma. It is postulated that ACE inhibition reduces the accumulation of AGE in diabetes partly by increasing the production and secretion of sRAGE into plasma.

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Section: Increases In Circulating Age Levels Are Accompanied By Decrementioning

confidence: 62%

Section: Human Plasma Samplesmentioning

confidence: 99%

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Modulation of Soluble Receptor for Advanced Glycation End Products by Angiotensin-Converting Enzyme-1 Inhibition in Diabetic Nephropathy

Forbes¹,

Thorpe²,

Thallas‐Bonke³

et al. 2005

Journal of the American Society of Nephrology

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196

129

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“…We acknowledge that this represents a paradigm shift for some. While it is clear that staging of nephropathy is an important means to stratify the risk of progressive kidney disease, albuminuria should be considered as a log-linear continuous variable for following the evolution of kidney disease in diabetes (14). For the same reasons, change in creatinine clearance was used as the primary outcome measure in patients with macroalbuminuria.…”

Section: Pooled Analysismentioning

confidence: 99%

Serum Lipids and the Progression of Nephropathy in Type 1 Diabetes

et al. 2006

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GIANCARLO VIBERTI, MD, FRCP 4PER-HENRIK GROOP, MD, DMSC 2 OBJECTIVE -Dyslipidemia contributes to the progression of microvascular disease in diabetes. However, different lipid variables may be important at different stages of nephropathy. This study examines the pattern of dyslipidemia associated with the progression of nephropathy in patients with type 1 diabetes.RESEARCH DESIGN AND METHODS -A total of 152 patients with type 1 diabetes were recruited in order to represent various phases of nephropathy. Patients were followed for 8 -9 years, during which time they received standard care. Renal progression was defined a priori as a doubling in albumin excretion (in patients with normo-or microalbuminuria) or a decline in creatinine clearance (in those with macroalbuminuria). A panel of lipid variables was determined and correlated with indexes of progression.RESULTS -In patients with normoalbuminuria (n ϭ 66), progression was associated with male sex (P Ͻ 0.05), borderline albuminuria (P ϭ 0.02), and LDL-free cholesterol (P ϭ 0.02). In patients with microalbuminuria (n ϭ 51), progression was independently associated with triglyceride content of VLDL and intermediate-density lipoprotein (both P Ͻ 0.05). In patients with macroalbuminuria (n ϭ 36), a significant decline in the renal function (Ͼ3 ml ⅐ min Ϫ1 ⅐ year Ϫ1 ) was independently associated with poor glycemic control, hypertension, and LDL size (P Ͻ 0.05). When all patients with progressive nephropathy were analyzed together, only LDL cholesterol was predictive on multivariate analysis (P Ͻ 0.05), which masked the importance of triglyceride enrichment in microalbuminuria.CONCLUSIONS -Lipid variables are associated with progression of diabetic kidney disease, but the relationship is not the same at all stages. This finding has implications for the design of renoprotective strategies and the interpretation of clinical trials in type 1 diabetes. Diabetes Care 29:317-322, 2006T he control of blood lipids is one of the cornerstones in the treatment of type 1 diabetes. Apart from effects on macrovascular outcomes (1), dyslipidemia potentially contributes to microvascular disease (2,3). Prospective studies have confirmed a link between serum lipids and nephropathy (4 -10), although lipid fractions measured in these studies have been limited, and parameters associated with kidney disease have not been consistently identified (8,9). It remains to be established which lipids or lipoproteins are most important in the pathogenesis of nephropathy and should therefore be targeted for intervention. Furthermore, it may be that different lipid variables are important at different stages of diabetic kidney disease. For example, triglycerides and cholesterol appeared to have different effects on the progression of nephropathy, depending upon the duration of diabetes (10). Consequently, this study makes a detailed examination of the pattern of dyslipidemia associated with the progression of nephropathy, at each stage of renal disease, in patients with type 1 diabetes followed fo...

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“…Approaches which focus on attenuating the intrarenal hemodynamic abnormalities associated with diabetes such as agents that interrupt the renin-angiotensin system (RAS), namely angiotensin converting enzyme-1 (ACEi) inhibitors (3) and angiotensin II (Ang II) receptor antagonists (4), respectively, are currently the most effective clinical interventions for the prevention and treatment of diabetic nephropathy, as assessed by urinary albumin excretion. Other known hypotensive agents without effects on the RAS do not confer the same degree of renoprotection in diabetic complications (5), implying that the nonhemodynamic mechanisms seen with RAS blockade, may be equally important contributors to their protective actions. Although poorly characterized in the diabetic context, these potentially downstream pathways are thought to include oxidative stress with both mitochondrial and cytosolic sources of reactive oxygen species (ROS) implicated in a range of diabetic vascular complications (6 -8).…”

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confidence: 99%

Combination Therapy with the Advanced Glycation End Product Cross-Link Breaker, Alagebrium, and Angiotensin Converting Enzyme Inhibitors in Diabetes: Synergy or Redundancy?

Coughlan¹,

Thallas‐Bonke²,

Pete³

et al. 2007

Endocrinology

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Blockade of advanced glycation end product (AGE) accumulation with alagebrium with concomitant angiotensin converting enzyme inhibition was tested for effects on renal function and on other postulated mediators of diabetic renal disease including the renin-angiotensin system, AGEs, mitochondrial and cytosolic oxidative stress, and intracellular signaling molecules. Sprague Dawley rats were rendered diabetic with streptozocin and followed consecutively for 32 wk with nondiabetic controls. Groups were treated with ramipril (1 mg/kg⅐d; wk 0 -32); alagebrium (10 mg/kg⅐d; wk 16 -32); or a combination of both. Although individual treatments had significant effects on albuminuria, no further improvements were seen with combination therapy. Changes in urinary vascular endothelial growth factor excretion mirrored those seen in albuminuria. Diabetes was associated with suppression of circulating angiotensin II in the context of increased circulating and renal levels of the AGE, carboxymethyllysine. All treatments attenuated circulating but not renal carboxymethyllysine levels. The renal gene expression of AGE receptor 1 and soluble receptor for advanced glycation end products were markedly reduced by diabetes and normalized with alagebrium. Diabetes induced renal mitochondrial oxidative stress, which was reduced with alagebrium. In the cytosol, both therapies were equally effective in reducing reactive oxygen species production. Increases in membranous protein kinase C activity in diabetes were attenuated by all treatments, whereas diabetes-associated increases in nuclear factor-B p65 translocation remained unaltered by any therapy. It is evident that renin-angiotensin system blockade and AGE inhibition have specific effects. However, many of their downstream effects appear to be similar, suggesting that their renoprotective benefits may ultimately involve common pathways and key points of convergence, which could be important targets for new therapies in diabetic nephropathy. (Endocrinology 148: 886 -895, 2007)

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Long-term comparison between perindopril and nifedipine in normotensive patients with type 1 diabetes and microalbuminuria

Cited by 70 publications

References 34 publications

Modulation of Soluble Receptor for Advanced Glycation End Products by Angiotensin-Converting Enzyme-1 Inhibition in Diabetic Nephropathy

Modulation of Soluble Receptor for Advanced Glycation End Products by Angiotensin-Converting Enzyme-1 Inhibition in Diabetic Nephropathy

Serum Lipids and the Progression of Nephropathy in Type 1 Diabetes

Combination Therapy with the Advanced Glycation End Product Cross-Link Breaker, Alagebrium, and Angiotensin Converting Enzyme Inhibitors in Diabetes: Synergy or Redundancy?

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