Urinary N-Acetyl-Beta-<i>D</i>-Glucosaminidase Activity in Children with Insulin-Dependent Diabetes mellitus

Abstract

Urinary N-acetyl-β -D-glucosaminidase (NAG) is a sensitive indicator of renal tubular injury. The aim of the study is to determine the status of urinary NAG excretion in Chinese children with insulin-dependent diabetes mellitus (IDDM) but without any clinical evidence of nephropathy, and to try to find the possible associated factors of such tubular injury if any. Thirty-one children (8 males and 23 females) with IDDM who have normal serum creatinine, 24-hour urinary creatinine clearance and urinary total protein excretion were enrolled in the study. The mean age of the patients was 11.6 ± 3.7 years. The random urinary NAG levels of the patients and the normal controls were 10.76 ± 6.32 and 3.65 ± 1.84 U/g Cr, respectively (p < 0.001). The diabetic patients were divided into 4 groups according to their duration of disease ( < 3, 3-5, 5-10 and 10-16 years). The random urinary NAG level of each group was significantly higher than that of the control group, but there was no statistically significant difference among any 2 of these 4 groups. No good correlation was noted in our study between urinary NAG and patients’ age (r = -0.23, p = 0.21), serum cholesterol (r = 0.04, p = 0.84), insulin dosage (r = 0.13, p = 0.49), 24-hour urinary creatinine clearance (r = -0.41, p = 0.085) or urinary total protein excretion (r = -0.28, p = 0.26). However, the plasma HbAlc level correlated significantly with urinary NAG (r = 0.50, p < 0.01). We concluded that urinary NAG is increased in Chinese IDDM children without any clinical evidence of nephropathy. Such increased excretion is correlated with the plasma HbAlc level. Our results suggest that there is tubular dysfunction in the early stage of IDDM children even before there is any clinical evidence of nephropathy, and urinary NAG may reflect glycemic control in such patients.

Diagnostic Value of the Aminopeptidase N, N-Acetyl-β-D-Glucosaminidase and Dipeptidylpeptidase IV in Evaluating Tubular Dysfunction in Patients with Glomerulopathies

“…[27] Urinary NAGA was found to be increased in children with insulin-dependent diabetes mellitus (IDDM) without any clinical evidence of nephropathy. [28] Such increased excretion correlated with the plasma HbAlc level. There is a tubular dysfunction in the early stage of IDDM children even before there is any clinical evidence of nephropathy, and urinary NAGA may reflect glycemic control in such patients.…”

“…Compared to healthy controls, urinary APN and NAGA were found significantly elevated in glomerulonephritis patients. [28] APN indicates very early tubular impairment and, in some cases, APN is elevated although NAGA is still within normal ranges. [13] In conclusion, damage of tubules in primary glomerulonephritis, lupus nephritis, and diabetic nephropathy is accompanied by a release of several tubular enzymes, with possible diagnostic and prognostic significance.…”

Increased Expression of Glutathione S- Transferase in Renal Proximal Tubules in the Early Stages of Diabetes: A Study of Type-2 Diabetes in the Akita Mouse Model

“…Previous studies reported that urinary excretion of N-acetylglucosaminidase as a sensitive marker of renal tubular damage was increased in patients in the early stages of type-1 [18, 19]and type-2 [20, 21]diabetes. These lines of evidence suggest that hyperglycemia may provide effects on renal tubular cells even in the early stages of diabetes.…”

Alteration of urinary sorbitol excretion in WBN-kob diabetic rats - treatment with an aldose reductase inhibitor

“…On the other hand, it has been reported that N-acetyl--glucosaminidase (NAG) activity in urine increased during the development of the early stages of diabetic nephropathy, and is correlated with the increase of urinary microalbumin and other parameters relevant to diabetes (UK Prospective Diabetes Study 1993, Hsiao et al 1996, Kato et al 1997, Yamanouchi et al 1998, Ishii et al 2001. Although NAG is widely distributed in various organs, it is especially concentrated in the epithelial cells of the renal proximal tubules (Price 1992).…”