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Role of Cystatin C in Renal Damage and the Optimum Cut-off Point of Renal Damage Among Patients with Type 2 Diabetes Mellitus

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Journal Exp Ther Med
Specialty Pathology
Date 2014 Aug 15
PMID 25120619
Citations 11
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Abstract

The aims of the present study were to evaluate the roles of serum cystatin C (SCysC) and urinary cystatin C (UCysC) in renal function impairment and investigate the optimum cut-off point for renal function impairment among patients with type 2 diabetes mellitus (DM). A total of 742 inpatients and outpatients with type 2 DM (age, 20-75 years) were enrolled in this population-based cross-sectional study. The levels of SCysC and UCysC were determined and the odds ratios (ORs) and 95% confidence interval (CIs) of the calculated risk ratios of the different renal damage indicators were obtained. The levels of UCysC, urinary β2-microglobulin (Uβ2-MG), urinary albumin (UALB) and SCysC in the renal function impairment groups were observed in the following order: GFR-C>GFR-B>GFR-A (P<0.05 or P<0.01). According to the levels of GFR were divided into 4 groups, group GFR-A ≥ 80ml/min, GFR-B group 50-80 ml/min, group Ccr-C 20-50 ml/min, group GFR-D <20 ml/min. Following adjustment for age and gender, multivariate correlation analysis results revealed that levels of Uβ2-MG, UCysC and UALB negatively correlated with the glomerular filtration rate (GFR; P<0.05 or P<0.01). In addition, the duration of DM and the levels of SCysC and serum uric acid were shown to positively correlate with the GFR (P<0.05 or P<0.01). ORs for early renal function impairment significantly increased from the DM duration category of four years (OR, 1.74; 95% CI, 1.54-1.92). Receiver operating characteristic analysis demonstrated that the optimum DM cut-off point was four years, in which 60.79% sensitivity and 69.66% specificity were observed. Therefore, UCsyC levels may be used as an efficient indicator for the evaluation of early renal function impairment among patients with type 2 DM. In addition, renal lesions may initially occur in the renal tubule and then form in the renal glomerulus of patients with type 2 DM.

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