Key result
Lack of metabolic syndrome correction in patients with type 2 diabetes was independently associated with an increased risk of developing microalbuminuria (HR 2.8; 95% CI 1.9-4.2; P<0.001).
Why the study?
Does correction of metabolic syndrome prevent the progression of diabetic nephropathy in individuals with type 2 diabetes?
Cohort
Does correction of metabolic syndrome prevent the progression of diabetic nephropathy in individuals with type 2 diabetes?
Correction of metabolic syndrome in patients with type 2 diabetes is associated with a slower progression of diabetic nephropathy, as evidenced by better preserved GFR and lower microalbuminuria.
Answers are grounded in this paper and cite their sources.
May support targeting metabolic syndrome in type 2 diabetes to lower microalbuminuria risk; leaves open causal effects on nephropathy progression.
BACKGROUND: Metabolic syndrome contributes to the development of albuminuria and to the decrease of glomerular filtration rate (GFR) in type 2 diabetes patients. The aim of this study was to analyze the effect of MS treatment on the progression of diabetic nephropathy (DN). METHODS: This was a retrospective and comparative cohort study. Baseline and follow-up data related to the presence of metabolic syndrome, microalbuminuria (mA), and GFR were obtained in individuals with type 2 diabetes. Subjects were classified in two groups: (1) With correction of metabolic syndrome and (2) without correction of metabolic syndrome at follow-up. Furthermore, they were stratified in four subgroups: (A) Without metabolic syndrome at baseline and at follow-up, (B) with metabolic syndrome and correction of metabolic syndrome, (C) without metabolic syndrome and development of metabolic syndrome, and (D) with metabolic syndrome and persistence of metabolic syndrome. RESULTS: Final GFR and mA were lower and higher, respectively, in group 2 versus 1 [89.8±3 2.3 vs. 98.3±32.0 mL/min, P=0.010, and 51.0 (13.5-195) vs. 7.9 (4-31) mg/day, P<0.001, respectively]. Lack of metabolic syndrome correction [hazard ratio (HR)=2.8, 95% confidence interval (CI) 1.9-4.2, P<0.001], being in subgroups C (HR=2.05, 95% CI 1.03-4.1, P=0.04) and D (HR=3.3, 95% CI 2.0-5.3, P<0.001), and the presence of two (HR=3.4, 95% CI 1.9-6.1, P<0.001), three (HR=5.0, 95% CI 2.5-9.9, P<0.001), and four (HR=4.2, 95% CI 1.5-12.1, P=0.006) metabolic syndrome components were independent factors associated with development of mA in Cox regression analysis adjusted for age, gender, baseline mA and GFR, glycosylated hemoglobin (HbA1c), hypertension, and obesity. CONCLUSIONS: Metabolic syndrome treatment and control are independently associated with a lesser progression of DN.
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Durán-Pérez et al. (2011) conducted a cohort in Type 2 diabetes with metabolic syndrome. Lack of metabolic syndrome correction vs. Correction of metabolic syndrome was evaluated on Development of microalbuminuria (HR 2.8, 95% CI 1.9-4.2, p=<0.001). Lack of metabolic syndrome correction in patients with type 2 diabetes was independently associated with an increased risk of developing microalbuminuria (HR 2.8; 95% CI 1.9-4.2; P<0.001).
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