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      Association of Metabolic Syndrome with Microalbuminuria in Non-Hypertensive Type 2 Diabetic Patients

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          Background: Several studies have shown that metabolic syndrome contributed to the development of incident chronic kidney disease in the general population. We evaluated the cross-sectional association between metabolic syndrome and microalbuminuria in patients with type 2 diabetes. We excluded patients with hypertension to distinguish the effects of metabolic syndrome from those of hypertension. Methods: A total of 642 non-hypertensive patients with type 2 diabetes were recruited. Metabolic syndrome was assessed according to the NCEP Guidelines and Asian-Pacific criteria for abdominal obesity. Results: Among all patients, 37.2% were diagnosed as having metabolic syndrome, and these patients had a higher prevalence of microalbuminuria than those without metabolic syndrome (19.7 vs. 13.6%, p = 0.044). There was a graded association between metabolic score and the prevalence of microalbuminuria (p = 0.006 for trend). After adjustment for sex, age, smoking status, C-reactive protein, and HbA<sub>1c</sub>, patients with metabolic syndrome had increased odds of 1.58 (95% CI 1.01–2.47) for microalbuminuria. An increment in metabolic score was found to increase the risk of microalbuminuria by 1.34-fold (95% CI 1.07–1.66, p = 0.008). Conclusion: This study demonstrated that metabolic syndrome was associated with an increased risk of microalbuminuria in non-hypertensive patients with type 2 diabetes.

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          Most cited references 11

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          Microalbuminuria predicts clinical proteinuria and early mortality in maturity-onset diabetes.

           C E Mogensen (1984)
          We studied whether microalbuminuria (30 to 140 micrograms of albumin per milliliter) would predict the later development of increased proteinuria and early mortality in Type II diabetics. During 1973, morning urine specimens of diabetic clinic patients 50 to 75 years of age whose disease had been diagnosed the age of 45 were examined for albumin level by radioimmunoassay. Seventy-six patients with albumin concentrations of 30 to 140 micrograms per milliliter were identified for long-term follow-up. They were compared with normal controls, diabetic patients with lower albumin concentrations (75 patients with concentrations less than 15 micrograms per milliliter and 53 with concentrations of 16 to 29 micrograms per milliliter), and 28 diabetic patients with higher concentrations (greater than 140). Age, duration of diabetes, treatment method, fasting blood glucose level, blood pressure, height, and weight were determined for the four diabetic groups. After nine years the group with albumin concentrations of 30 to 140 micrograms per milliliter was more likely to have clinically detectable proteinuria (greater than 400 micrograms per milliliter) than were the groups with lower concentrations. Mortality was 148 per cent higher in this group than in normal controls--comparable to the increase (116 per cent) in the group with heavy proteinuria (albumin levels greater than 140 micrograms per milliliter). In addition, mortality was increased 76 per cent in the group with albumin levels of 16 to 29 micrograms per milliliter and 37 per cent in the group with levels below 15. We conclude that microalbuminuria in patients with Type II diabetes is predictive of clinical proteinuria and increased mortality.
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            The metabolic syndrome, inflammation, and risk of cognitive decline.

            Several studies have reported an association between the metabolic syndrome and cardiovascular disease. Despite an increasing awareness that cardiovascular risk factors increase risk of cognitive decline and dementia, there are few data on the metabolic syndrome and cognition. To determine if the metabolic syndrome is a risk factor for cognitive decline and if this association is modified by inflammation. A 5-year prospective observational study conducted from 1997 to 2002 at community clinics at 2 sites. A total of 2632 black and white elders (mean age, 74 years). Association of the metabolic syndrome (measured using National Cholesterol Education Program guidelines) and high inflammation (defined as above median serum level of interleukin 6 and C-reactive protein) with change in cognition (Modified Mini-Mental State Examination [3MS]) at 3 and 5 years. Cognitive impairment was defined as at least a 5-point decline. Compared with those without the metabolic syndrome (n = 1616), elders with the metabolic syndrome (n = 1016) were more likely to have cognitive impairment (26% vs 21%, multivariate adjusted relative risk [RR], 1.20; 95% confidence interval [CI], 1.02-1.41). There was a statistically significant interaction with inflammation and the metabolic syndrome (P = .03) on cognitive impairment. After stratifying for inflammation, those with the metabolic syndrome and high inflammation (n = 348) had an increased likelihood of cognitive impairment compared with those without the metabolic syndrome (multivariate adjusted RR, 1.66; 95% CI, 1.19-2.32). Those with the metabolic syndrome and low inflammation (n = 668) did not exhibit an increased likelihood of impairment (multivariate adjusted RR, 1.08; 95% CI, 0.89-1.30). Stratified multivariate random-effects models demonstrated that participants with the metabolic syndrome and high inflammation had greater 4-year decline on 3MS (P = .04) compared with those without the metabolic syndrome, whereas those with the metabolic syndrome and low inflammation did not (P = .44). These findings support the hypothesis that the metabolic syndrome contributes to cognitive impairment in elders, but primarily in those with high level of inflammation.
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              Clinical practice. Nephropathy in patients with type 2 diabetes.


                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                July 2007
                22 May 2007
                : 106
                : 3
                : c98-c103
                aDepartment of Medicine, Division of Nephrology, and bCenter for Health Promotion, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
                102996 Nephron Clin Pract 2007;106:c98–c103
                © 2007 S. Karger AG, Basel

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                Figures: 2, Tables: 3, References: 28, Pages: 1
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