Effect of antidiabetic medications on microalbuminuria in patients with type 2 diabetes

Yanagawa, Tatsuo; Araki, Atsushi; Sasamoto, Kazuo; Shinzaki, Shinichiro; Yamanouchi, Toshikazu

doi:10.1016/j.metabol.2003.10.025

Cited by 32 publications

(22 citation statements)

References 22 publications

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“…Of course, during this phase albuminuria may also be reduced. 6,13 Therefore, in contrast with our findings, a positive correlation between UACR and endocan could have been detected. Patients with microalbuminuria in our study had insignificantly lower endocan than patients with normoalbuminuria.…”

Section: 12contrasting

confidence: 99%

Endocan and albuminuria in type 2 diabetes mellitus

et al. 2016

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Background: Endocan is a newly identified proteoglycan released from endothelium, stimulating angiogenesis and when increased, indicates endothelial activation (inflammation). Our aim was to examine the association between serum endocan levels and urine albumin-creatinine ratio (UACR). Method: One hundred and thirty-seven patients with type 2 diabetes mellitus and normal serum creatinine who had no co-morbidities other than hypertension, diabetic nephropathy, retinopathy, or neuropathy were divided into normoalbuminuria (G1), microalbuminuria (G2), and macroalbuminuria (G3) groups and compared cross-sectionally regarding serum endocan levels. Result: There were 55, 47, and 35 patients in G1, G2, and G3, respectively. The groups were comparable in terms of gender, age, duration of diabetes, diabetic neuropathy/retinopathy, fasting glucose, HbA1c, serum creatinine level, and eGFR. Patients in G3 had significantly higher blood pressure but lower serum albumin and endocan levels. UACR showed a negative bivariate correlation with serum endocan levels (r ¼ À.282, p ¼ .001). There was bivariate positive correlation between endocan and systolic blood pressure (r¼.185, p ¼ .030). In linear regression analysis, UACR was negatively correlated with endocan while positively correlated with systolic blood pressure, duration of diabetes, and platelet distribution width. Conclusion: Patients with macroalbuminuria had lower endocan levels, and increasing UACR was associated with decreasing serum endocan levels. Despite the occurrence of angiogenesis and glomerular hypertrophy in the early phase of diabetic nephropathy, ensuing significant renal injury over time may reduce the expression of endocan. Serum endocan levels may represent a novel marker for nephropathy progression.

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Section: 12contrasting

confidence: 99%

Endocan and albuminuria in type 2 diabetes mellitus

et al. 2016

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“…Urinary albumin excretion decreased in subjects with microalbuminuria and type 2 diabetes who were randomized to 4 mg twice daily of rosiglitazone for 26 weeks [33] or 52 weeks [41]. However, Yanagawa et al [42] were unable to find superior protection through pioglitazone compared to another nonglitazone oral hypoglycemic agent, glicazide. Finally, Nakamura et al [34] studied 32 normotensive patients with type 2 diabetes mellitus with microalbuminuria (N = 16) or macroalbuminuria (N = 16) randomly assigned in equal numbers to troglitazone or glibenclamide.…”

Section: Discussionmentioning

confidence: 98%

A pilot randomized controlled trial of renal protection with pioglitazone in diabetic nephropathy

Agarwal¹,

Saha²,

Battiwala³

et al. 2005

Kidney International

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“…Within the limits of this study, the data presented here suggest that reductions in biochemical risk factors and blood pressure may be the dominant contributors to such vascular benefits rather than changes in insulin resistance. Data suggest that pioglitazone and other thiazolidinediones decrease C-reactive protein levels (18), microalbuminuria (36), arterial pulse-wave velocity (18), systolic and diastolic blood pressure (17), and increase adiponectin levels (18), each of which is associated with cardiovascular risk reduction. These data provide rationale for ongoing research to determine the nature of the effect of this class of agents on the cardiovascular system.…”

Section: Conclusion -The Major Finding Of This Pilot Study Was That mentioning

confidence: 99%

Effect of a Peroxisome Proliferator–Activated Receptor-γ Agonist on Myocardial Blood Flow in Type 2 Diabetes

et al. 2005

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OBJECTIVE -The relationship between coronary endothelial function and insulin resistance remains speculative. We sought to determine whether pioglitazone, an insulin-sensitizing peroxisome proliferator-activated receptor (PPAR)-␥ agonist, improves cardiac endothelial function in individuals with type 2 diabetes.RESEARCH DESIGN AND METHODS -Sixteen subjects with insulin-treated type 2 diabetes and without overt cardiovascular disease were randomly assigned to receive either 45 mg of pioglitazone or matching placebo for 3 months. Rest and adenosine-stimulated myocardial blood flow (MBF) were quantified with [13 N]ammonia and positron emission tomography at baseline and study conclusion.RESULTS -After 3 months, HbA 1c levels dropped by 0.68% in the pioglitazone group and increased by 0.17% in the placebo group (P ϭ 0.009 for difference between groups). Triglyceride (Ϫ93 vs. Ϫ39 mg/dl, P ϭ 0.026) and HDL concentrations (ϩ4.8 vs. Ϫ6.0 mg/dl, P ϭ 0.014) improved significantly in the pioglitazone group compared with placebo. Despite these favorable changes, there was no demonstrable change in baseline MBF (Ϫ0.05 Ϯ 0.24 vs. Ϫ0.09 Ϯ 0.24 ml ⅐ min Ϫ1 ⅐ g Ϫ1 , P ϭ 0.45), adenosine-stimulated MBF (0.10 Ϯ 0.75 vs. 0.14 Ϯ 0.31 ml ⅐ min Ϫ1⅐ g Ϫ1 , P ϭ 0.25), or coronary flow reserve (0.45 Ϯ 1.22 vs. 0.35 Ϯ 0.72 ml ⅐ min Ϫ1 ⅐ g Ϫ1 , P ϭ 0.64) after 12 weeks of exposure to pioglitazone or placebo, respectively. Regression analysis revealed that lower glucose concentration at the time of the study was associated with higher coronary flow reserve (P ϭ 0.012).CONCLUSIONS -Pioglitazone treatment for 12 weeks in subjects with insulin-requiring type 2 diabetes had no demonstrable effect on coronary flow reserve despite metabolic improvements. Higher ambient glucose levels contribute to impaired vascular reactivity in individuals with diabetes. Diabetes Care 28:1145-1150, 2005A therosclerotic vascular disease and its sequelae remain the primary causes of mortality in patients with diabetes, accounting for 65-75% of deaths (1). Recent attention has focused on functional abnormalities of the endothelium as an early step in the pathogenesis of diabetic heart disease (2,3). Notably, studies on individuals with diabetes have demonstrated a consistently higher myocardial blood flow (MBF) at rest and impaired myocardial vasodilation capacity (4).Endothelial dysfunction occurs when endogenous vasoconstrictors such as endothelin and angiotensin II dominate the action of naturally occurring vasodilators such as nitric oxide, an imbalance linked to known cardiovascular risk factors (5-7). Importantly, measures of endothelial dysfunction predict subsequent cardiovascular events (8). Insulin resistance has emerged as a putative common link between diabetes and endothelial dysfunction. Those with insulin resistance demonstrate impaired endothelial function (7,9) even before diabetes is diagnosed, and insulin induces vasodilation via endothelial nitric oxide release (10,11).Thiazolidinediones activate the nuclear receptor peroxisome proliferatoractiv...

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Effect of antidiabetic medications on microalbuminuria in patients with type 2 diabetes

Cited by 32 publications

References 22 publications

Endocan and albuminuria in type 2 diabetes mellitus

Endocan and albuminuria in type 2 diabetes mellitus

A pilot randomized controlled trial of renal protection with pioglitazone in diabetic nephropathy

Effect of a Peroxisome Proliferator–Activated Receptor-γ Agonist on Myocardial Blood Flow in Type 2 Diabetes

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