The purpose of this study was evaluating the early diagnostic value of two specific tubular markers neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in diabetes nephropathy. Patients and Methods: Cross-sectional study was carried in three groups of patients from 10/2017 to 10/2018 in Military Hospital 103. Group I included 30 healthy peoples with estimated glomerular filtration rate (eGFR) >60 mL/min/1.73 m 2 and urine albumin creatinine ratio (uACR) <30 mg/g. Group II included 30 type 2 diabetic patients having uACR <30 mg/g, eGFR >60 mL/min/1.73 m 2. Group III included 30 type 2 diabetic patients having uACR >30 mg/g, eGFR >60 mL/min/1.73 m 2. Results: Urine KIM-1 and NGAL increased progressively from control group (57.29 ± 25.91 pg/mL; 25.71 ± 13.69 ng/mL) to the group of diabetic patients with uACR <30 mg/g (167.06 ± 44.01 pg/mL; 37.42 ± 10.89 ng/mL) and the group of diabetic patients with uACR ≥30 mg/g) (p < 0.05). There were moderate correlations between KIM-1 (r = 0.48, p < 0.05) and NGAL (r = 0.45, p < 0.05) with uACR. There was a mild correlation between KIM-1 and NGAL (r = 0.29, p < 0.05). KIM-1 and NGAL are the independent tests to detect diabetic nephropathy. The sensivity and specificity of KIM-1 with cutoff value of 174.95 pg/mL were 62.37% and 73.48%, respectively; the sensivity and specificity of NGAL with cutoff value of 35.2 ng/mL were 60.45% and 70.37%, respectively. Conclusion: KIM-1 and NGAL in urine are independent markers for early diagnostic diabetic nephropathy.
Background: Chronic kidney disease (CKD) is an increasingly common disease worldwide and has become a global health problem, especially in Vietnam. Cystatin C is a marker for the detection, classification, and prognosis of CKD. Cystatin C is filtered entirely through the glomerular membrane, reabsorbed, and metabolized completely in the renal tubules. In case of damage to the kidneys, glomerular filtration rate declines, and some substances increase in the blood, such as cystatin C. The concentration of cystatin C changes with damage to the renal system. Objectives: This study aimed to estimate the concentration of cystatin C and its variation in the different stages of CKD. Methods: A descriptive, cross-sectional study was conducted on 40 healthy individuals and 137 patients with CKD grade III, IV, and V in 103 Hospital. The concentration of cystatin C was estimated in all subjects. Results: Cystatin C plasma levels were significantly higher in the CKD group (9.17 ± 3.75 mg/L) than in the control group (0.82 ± 0.12 mg/L). Cystatin C plasma levels increased linearly with the serious kidney failure as the stage of CKD. Conclusions: Cystatin C is an effective marker for estimating kidney damage in CKD.
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