Efficacy of urinary N-acetyl-β-D-glucosaminidase to evaluate early renal tubular damage as a consequence of type 2 diabetes mellitus: a cross-sectional study

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• 作者：Dhara N. Patel ; Kiran Kalia
• 关键词：Urinary N ; acetyl ; β ; d ; glucosaminidase ; Serum N ; acetyl ; β ; d ; glucosaminidase ; Proximal tubular damage ; Type 2 diabetes mellitus ; Diabetic nephropathy
• 刊名：International Journal of Diabetes in Developing Countries
• 出版年：2015
• 出版时间：November 2015
• 年：2015
• 卷：35
• 期：3-supp
• 页码：449-457
• 全文大小：481 KB
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• 作者单位：Dhara N. Patel (1)
  Kiran Kalia (1) (2)
  
  1. Laboratory of Biochemistry, B.R.D. School of Biosciences, Sardar Patel University, Sardar Patel Maidan, Vadtal Road, Satellite Campus, Post Box No. 39, Vallabh Vidyanagar, 388 120, Gujarat, India
  2. National Institute of Pharmaceutical Education and Research (NIPER-G); Gandhinagar, c/o B V Patel PERD Centre, SG Highway, Thaltej, Ahmedabad, 380 054, Gujarat, India
  
• 刊物主题：Medicine/Public Health, general; General Practice / Family Medicine; Health Administration; Diabetes;
• 出版者：Springer India
• ISSN：1998-3832

文摘

We assessed the prognostic accuracy of urinary N-acetyl-β-D-glucosaminidase (NAG), an early proximal tubular damage marker for the onset of diabetic nephropathy. The study included 491 eligible participants with 76 healthy controls, 194 type 2 diabetes mellitus (T2DM) patients with 0–5, 5–10, 10–15, and 15–20 years of T2DM duration, 71 microalbuminuric patients, 100 diabetic nephropathy patients, and 50 non-diabetic nephropathy patients. Fasting glucose, serum fructosamine, HbA1C, urinary microalbumin, serum creatinine, estimated glomerular filtration rate (eGFR), serum NAG, and urinary NAG were estimated. We compared urinary NAG activity with other well-established markers of diabetic nephropathy like microalbuminuria, eGFR, and serum creatinine. Urinary NAG excretion was increased by 8 and 12 folds in T2DM patients of 10–15 and 15–20 years of diabetes duration (p < 0.0001), respectively, without the appearance of microalbuminuria. The urinary NAG activity increased 16 and 18 fold in moderately increased albuminuria and diabetic nephropathy patients, respectively (p < 0.0001), without any change in non-diabetic nephropathy patients. A cutoff value of 3 U/L of urinary NAG has demonstrated a sensitivity of 96.1 % and a specificity of 100 % discriminating healthy controls from patients with T2DM duration of 10–15 years (AUC 1.000) and 15–20 years (AUC 0.999); microalbuminuria (AUC 0.999), and diabetic nephropathy (AUC 1.000). Urinary NAG excretion gradually increases with the increase in duration of diabetes and appeared much before the microalbuminuria, decreased eGFR, and increased serum creatinine. Thus, the urinary NAG may be considered as a potential site-specific early tubular damage marker leading to diabetic nephropathy.