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Purpose: Adiponectin an adipokine, produced by mature adipocyte, has an important effect on several aspects of endothelial function, including leukocyte adhesion (mediated by adhesion molecules like intercellular adhesion molecule 1 (ICAM1) endothelial cell selective adhesion molecule ESAM). Recently, it has been linked to vascular endothelial growth factor (VEGF)-modulated angiogenesis. ESAM might also be involved in modulating VEGF-dependent actions. We studied relationship of adiponectin to ESAM, ICAM1, and VEGF in type 2 diabetic patients (T2DP) with or without microvascular complications., Methods: Incident T2DP referred for nephrologic evaluation were included (patients with no nephropathy or stage 1-4 nephropathy). T2DP with stage 5 chronic kidney disease (CKD) were selected from a dialysis center. Clinical, standard laboratory assessment and adiponectin, ESAM, ICAM1, and VEGF (ELISA) were recorded., Results: Eighty-seven patients were included, 15 had no CKD, 30 with stage 1 or 2 CKD, 20 with stage 3 or 4 CKD and 22 patients on dialysis. ESAM was higher in patients with CKD than in those without CKD (p = 0.02), adiponectin, ICAM1, and VEGF were similar. Adiponectin correlated in univariate analysis to ESAM (r = 0.32, p = 0.002), ICAM1 (r = 0.23, p = 0.038), and CRP (r = 0.31, p = 0.012), and inversely to serum albumin (r = - 0.57, < 0.0001). In predialysis patients, adiponectin also correlated to albuminuria (r = 0.54, p < 0.0001) and glomerular filtration rate (r = - 0.46, p = 0.0001). In multivariate regression ESAM (p = 0.04), VEGF (p = 0.03), and albumin (p < 0.0001) are significant predictors of adiponectin. None of these cytokines were different when comparing patients with and without retinopathy., Conclusion: Adiponectin is directly linked to adhesion molecules and VEGF in T2DP.

Purpose: Adiponectin may be beneficial in incipient chronic kidney disease by antagonizing oxidative stress. We evaluated adiponectin, malondialdehyde (MDA), and superoxide dismutase (SOD), in type 2 diabetes mellitus patients (T2DP) with and without incipient nephropathy., Methods: T2DP with glomerular filtration rate (GFR) >30 ml/min were compared with 20 healthy controls. Clinical and laboratory evaluations, levels of MDA (fluorimetric thiobarbituric test), SOD (cytochrome reduction method) and adiponectin (ELISA) were obtained., Results: Sixty-four patients (GFR 91.44 ± 38.50 ml/min, urinary albumin-to-creatinine ratio [UACR] 20.81 [4.64-72.88 mg/g]) were included. MDA was higher in T2DP than in controls: 3.97 (2.43-4.59) versus 1.35 (1.16-1.81) nmol/ml, p < 0.0001. MDA correlated with glycated hemoglobin (r = 0.40, p = 0.001), adiponectin (r = -0.28, p = 0.03), systolic blood pressure (r = -0.28, p = 0.03) and SOD (r = -0.35, p = 0.005); adiponectin (p = 0.01) and glycated hemoglobin (p = 0.02) remained significant predictors of MDA in multiple regression analysis. SOD was negatively correlated with glycemia (r = -0.71, p < 0.0001) and glycated hemoglobin (r = -0.5, p < 0.0001). When patients were divided according to a ROC-derived adiponectin cutoff of 8.9 µg/ml, patients with higher adiponectin had lower MDA, [2.55 (2.35-3.60) vs. 4.10 (2.89-5.31) nmol/ml, p = 0.005] but similar SOD levels. In T2DP with nephropathy (GFR < 60 ml/min or UACR > 30 mg/g), the correlation of adiponectin with MDA was stronger, (r = -0.51, p = 0.004) confirmed in multiple regression analysis (p = 0.03). Adiponectin was not correlated with MDA, and SOD was inversely related to MDA in patients without nephropathy., Conclusion: Adiponectin is a significant predictor of MDA in early diabetic nephropathy, whereas SOD strongly depends only on glycemic control and is not directly related to adiponectin.

Background: Adiponectin, an anti-inflammatory and insulin-sensitizing cytokine, has been shown to reduce proteinuria and glomerulosclerosis in experimental models. We assessed the relationship of plasma adiponectin to the progression of kidney disease in type 2 diabetes (T2D) patients., Methods: T2D nonnephrotic patients with glomerular filtration rate (GFR) >30 ml/min and without acute cardiovascular/inflammatory conditions were included. Laboratory standard evaluation, urinary albumin/creatinine ratio (UACR), total plasma adiponectin, and CRP (C-reactive protein) were determined at inclusion and the end of study., Results: Eighty-six patients (62.79% male) were followed up for 20.53±5.46 months. Baseline GFR was 72.85±26.29 ml/min and UACR was 20.53 (interquartile range 6.82-86.39) mg/g. At baseline adiponectin was significantly correlated to UACR (r =0.40, p =0.0001), HDL cholesterol (r =0.30, p =0.005), GFR (r =- 0.23, P =0.04), body mass index (BMI) (r =- 0.26, P =0.02) and waist circumference (r =-0.27, p =0.01). In multiple regression UACR (p =0.0003) and BMI (p =0.03) were significantly related to baseline adiponectin. The progression of kidney disease was estimated as the difference (D) between end and baseline UACR/month and between end and baseline GFR/month. None of the baseline parameters correlated to ΔGFR, but adiponectin inversely (r =- 0.26, p =0.02) correlated to ΔUACR. In multiple regression only adiponectin (p <0.0001) predicted ΔUACR. A computed progression index (PI) resulting from a linear combination of GFR and UACR was also used to assess progression. Baseline adiponectin was significantly correlated to ΔPI between end of study and baseline (r =- 0.43, p <0.0001), and predicted ΔPI in multiple regression (p =0.009)., Conclusion: Low plasma adiponectin predicts progression of kidney disease in T2D patients.

Aims: Our study addressed the influence of early inflammatory stages of diabetic kidney disease: leukocyte adhesion and monocyte activation (as assessed by intercellular leukocyte adhesion molecule-ICAM-1 and monocyte chemoatractant protein-MCP-1) on the degree of albuminuria. Plasma levels of adiponectin, a possible anti-inflammatory counteracting mechanism, were also studied in correlation to the above-mentioned cytokines., Methods: 79 consecutive type 2 diabetic outpatients and 46 controls were included. Routine laboratory analysis, urinary albumin to creatinine ratio (uACR), plasma adiponectin, plasma ICAM-1 and urinary MPC-1 were assessed., Results: In multiple regression ICAM-1 (p=0.004) and adiponectin (p=0.04) were the main determinants of uACR. Plasma adiponectin positively correlated to ICAM-1 (p=0.03, r=0.24). In albuminuric patients (uACR ≥30 mg/g) plasma adiponectin was significantly higher compared to normoalbuminuric ones (uACR <30 mg/g). In albuminuric patients the main determinants of uACR were plasma ICAM-1 and adiponectin. In multiple regression ICAM-1 is the only one that retains statistical significance (p=0.02). Urinary MCP-1 did not correlate to uACR., Conclusions: In our type 2 diabetic patients, plasma levels of ICAM-1 and adiponectin are predictive for albuminuria. Urinary MCP-1 does not correlated to uACR. Plasma adiponectin positively correlates to adhesion molecule ICAM-1 in our cohort., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Introduction. Experimental and clinical studies suggest an inverse relationship between adiponectin and oxidative stress. In this study we evaluated the relationship between serum adiponectin and oxidative stress in patients with type 2 diabetes mellitus with diabetic neuropathy. Material and methods. We included in this study 26 patients with type 2 diabetes mellitus and diabetic neuropathy, from the outpatient settings of the Clinic of Nephrology Mihai Manasia Cluj and 48 patients with type 2 diabetes without diabetic neuropathy. Exclusion criteria were: chronic renal disease other than diabetic nephropathy, diabetic nephropathy stage 4-5 KDOQI, the presence of acute inflammatory/infectious, uncontrolled hypertension. Results. In patients with neuropathy plasma adiponectin was significantly correlated with lipid peroxides-malondialdehyde r=-0.42, p=0.03, with catalase r=0.56, p=0.009, with high-density lipoprotein cholesterol r=0.53, p=0.005 and glycated hemoglobin r=-0.54, p=0.005. Lipid peroxides - malondialdehyde was significantly correlated with age r=-0.46, p=0.02, glycated hemoglobin r=-0.54, p=0.005; abdominal circumference r=-0.39, p=0.05. Superoxide dismutase was significantly correlated with blood glucose r=-0.84, p<0.001. In multivariate linear regression adiponectine was dependent of lipid peroxides - malondialdehyde (p=0.04), body mass index (p=0.002), high-density lipoprotein cholesterol (p=0.002) and glycated hemoglobin (p<0,001). In patients without neuropathy, multivariate linear regression found that adiponectine was dependent of urinary albumin/urinary creatinin report (p<0.001), high-density lipoprotein cholesterol (p<0.001), body mass index (p=0.009) and C-reactive protein (p=0.001). There were no significant differences in levels of adiponectin and oxidative stress parameters between diabetic neuropathy and without neuropathy group. Conclusion. In patients with diabetes mellitus type 2 and diabetic neuropathy, low level of oxidative stress was correlated with high level of adiponectin. [ABSTRACT FROM AUTHOR]

Background: Previous reports associated ADIPOQ 276G>T polymorphism with plasma adiponectin levels and diabetes. Our objective was to study this polymorphism in type 2 diabetes (T2D) Romanian patients and to assess its influence on plasma adiponectin levels; possible link to prevalence of T2D was also addressed. Design: Case control study Material and Methods: Consecutive T2D patients, age and sex matched controls were genotyped for the 276 ADIPOQ locus. Medical history, laboratory evaluation, plasma adiponectin were assessed. Outcomes: 105 T2D patients and 48 controls were included. Adiponectin was higher in controls (17.04±3.02 µg/ml) than in T2D patients (10.32±1.16 µg/ml), difference failed to reach significance (p=0.06). Genotype distribution wasn't different between T2D patients and controls. 44 (41.90%) of T2D patients had GG genotype, 51 (48.57%) GT and 10 (9.52%) TT genotype. Adiponectin was higher (19.03±3.46 µg/ml) in diabetic TT allele carriers than in GT (9.96±1.76 µg/ml) or GG patients (8.71±1.60 µg/ml) p=0.003. In controls, 28 (58.33 %) subjects were carriers of the GG genotype, 16 (33.33%) had GT genotype and 4 (8.33%) had TT genotype. There weren't significant differences in the studied parameters between different genotypes in the control group. Logistic regression disclosed age p=0.0001 (OR 1.086; CI 1.041/1.133), waist circumference p=0.00049 (OR 1.084; CI 1.036/1.135), adiponectinemia p=0.036 (OR 0.963; CI 0.929/0.998) but not genotype as predictors for the presence of diabetes. Conclusion: Presence of the TT allele at the 276 locus of the ADIPOQ gene is associated with higher plasma adiponectin levels in type 2 diabetes patients. Plasma adiponectin, and not genotype at the 276 locus is predictive for the presence of T2D. [ABSTRACT FROM AUTHOR]

Background: Adiponectin, an insulin-sensitizing, anti-inflammatory and antiatherogenic adipokine, seems to conserve its protective effect against cardiovascular complications in dialysis patients. In diabetic dialysis patients however results are less consistent, higher adiponectin levels being associated with mortality. We intend to study the prognostic value of plasma adiponectin for atherosclerotic complications and all-cause mortality in type 2 diabetic patients on hemodialysis in a multicenter trial; we hereby present our pilot study. Material and methods: All (28) diabetic patients on maintenance hemodialysis in our center were included in the study. History, clinical data, routine laboratory assessment and total plasma adiponectin were obtained. Patients were compared to a control group of 20 nondiabetic hemodialysis patients. During 1 year of follow-up, new occurrence of cardiovascular complications due to atherosclerosis (myocardial infarction and revascularization, amputation or revascularization due to arteriosclerosis obliterans, stroke) and all-cause mortality were recorded. Results: Type 2 diabetic dialysis patients had lower adiponectin levels than dialysis controls (21.08±3.17/ml versus 39.00±10.11μg/ml, p=0.03). In simple regression, adiponectin was correlated to body mass index (r=-0.43, p=0.01) and serum triglycerides (r=-0.62, p=0.0003); in multiple stepwise regression, triglycerides remained the only predictor of plasma adiponectin (p=0.01). Adiponectin levels were higher in women than in men (28.73±5.76 μg/ ml versus 15.33±2.88 μg/ml, p=0.03). There was a statistically significant difference in plasma adiponectin levels between patients with proliferative retinopathy and patients without this condition (27.22±4.87 μg/ ml versus 16.46±3.91 μg/ml, p=0.02). Patients with new onset of cardiovascular events had lower adiponectin levels than controls (12.76±3.52 μg/ml versus 23.34±3.81 μg/ml but the difference did not reach statistical significance, probably due to the small number of patients. Baseline adiponectin was higher in deceased patients than in survivors (29.87±10.32 μg/ml versus 19.61±3.29 μg/ml); again, statistical significance was not reached due to the small cohort. The number of patients to be included in the multicenter trial in order to attain statistical significance for each arm of the above mentioned comparisons was calculated. Conclusions: In diabetic patients treated with hemodialysis, lower adiponectin levels were found in patients with new onset of complications of atherosclerosis, while increased adiponectin might predict all-cause mortality. Further large-scale prospective studies are required to confirm these findings. [ABSTRACT FROM AUTHOR]