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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- Published online on: June 30, 2014 https://doi.org/10.3892/etm.2014.1815
- Pages: 887-892
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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.
