Urinary N -acetyl-β- d -glucosaminidase, an early marker of diabetic kidney disease, might reflect glucose excursion in patients with type 2 diabetes

So Ra Kim, Yong Ho Lee, Sang Guk Lee, Eun Seok Kang, Bong Soo Cha, Jeong Ho Kim, byungwan lee

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Abstract

Recently, several renal tubular damage markers have gained considerable attention because of their clinical implications as sensitive and specific biomarkers for early stage diabetic kidney disease. However, little is known about the demographic and glucometabolic factors affecting levels of urinary N-acetyl-β-d-glucosaminidase (NAG), a marker of proximal tubular damage, in type 2 diabetes mellitus (T2DM). The aim of this study was to investigate the clinical relevance of urinary NAG with regard to demographic and glucometabolic parameters, as well as nephropathic parameters, by comparing the glomerulopathic marker of albuminuria. In this retrospective cross-sectional study, we enrolled a total of 592 patients with either prediabetes (N = 29) or T2DM (N = 563). Glucometabolic parameters (glucose, hemoglobin A1c, glycated albumin [GA], insulin, C-peptide, homeostasis model assessment [HOMA] of insulin resistance, HOMA-β, postprandial C-peptide-to-glucose ratio [PCGR], and urinary glucose-to-creatinine ratio) and nephropathic parameters (urinary NAG, albumin-to-creatinine ratio [ACR], and estimated glomerular filtration rate) were measured. The levels of urinary NAG showed moderate positive correlation with the levels of urinary ACR in T2DM (r = 0.46). In correlation analysis, urinary NAG was more strongly correlated with body mass index (BMI) (r = -0.22; P < 0.001 vs. r = -0.02; P = 0.74), plasma stimulated glucose (r = 0.25; P < 0.001 vs. r = 0.08; P = 0.10), GA (r = 0.20; P < 0.001 vs. r = 0.13; P = 0.01), PCGR (r = -0.17; P = 0.001 vs. r = -0.09; P = 0.11), and HOMA-β (r = -0.10; P = 0.05 vs. r = -0.02; P = 0.79) than urinary ACR. In multiple regression analysis, age, lower BMI, stimulated glucose, GA, and urinary ACR predicted increased urinary NAG. In conclusion, increase in urinary NAG may be related to glycemic parameters reflecting glucose fluctuation and decreased insulin secretory capacity in patients with T2DM. Further longitudinal, prospective studies are needed to investigate a causal relationship between glucose fluctuations, renal tubular damage, and other vascular complications of diabetes.

Original languageEnglish
Article numbere4114
JournalMedicine (United States)
Volume95
Issue number27
DOIs
Publication statusPublished - 2016 Jul 1

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Hexosaminidases
Diabetic Nephropathies
Type 2 Diabetes Mellitus
Glucose
Creatinine
C-Peptide
Albumins
Homeostasis
Body Mass Index
Demography
Kidney
Prediabetic State
Albuminuria
Diabetes Complications
Glomerular Filtration Rate
Blood Vessels
Longitudinal Studies
Insulin Resistance
Hemoglobins
Cross-Sectional Studies

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

@article{78a9446f6278443e8e6e914fdc58ad22,
title = "Urinary N -acetyl-β- d -glucosaminidase, an early marker of diabetic kidney disease, might reflect glucose excursion in patients with type 2 diabetes",
abstract = "Recently, several renal tubular damage markers have gained considerable attention because of their clinical implications as sensitive and specific biomarkers for early stage diabetic kidney disease. However, little is known about the demographic and glucometabolic factors affecting levels of urinary N-acetyl-β-d-glucosaminidase (NAG), a marker of proximal tubular damage, in type 2 diabetes mellitus (T2DM). The aim of this study was to investigate the clinical relevance of urinary NAG with regard to demographic and glucometabolic parameters, as well as nephropathic parameters, by comparing the glomerulopathic marker of albuminuria. In this retrospective cross-sectional study, we enrolled a total of 592 patients with either prediabetes (N = 29) or T2DM (N = 563). Glucometabolic parameters (glucose, hemoglobin A1c, glycated albumin [GA], insulin, C-peptide, homeostasis model assessment [HOMA] of insulin resistance, HOMA-β, postprandial C-peptide-to-glucose ratio [PCGR], and urinary glucose-to-creatinine ratio) and nephropathic parameters (urinary NAG, albumin-to-creatinine ratio [ACR], and estimated glomerular filtration rate) were measured. The levels of urinary NAG showed moderate positive correlation with the levels of urinary ACR in T2DM (r = 0.46). In correlation analysis, urinary NAG was more strongly correlated with body mass index (BMI) (r = -0.22; P < 0.001 vs. r = -0.02; P = 0.74), plasma stimulated glucose (r = 0.25; P < 0.001 vs. r = 0.08; P = 0.10), GA (r = 0.20; P < 0.001 vs. r = 0.13; P = 0.01), PCGR (r = -0.17; P = 0.001 vs. r = -0.09; P = 0.11), and HOMA-β (r = -0.10; P = 0.05 vs. r = -0.02; P = 0.79) than urinary ACR. In multiple regression analysis, age, lower BMI, stimulated glucose, GA, and urinary ACR predicted increased urinary NAG. In conclusion, increase in urinary NAG may be related to glycemic parameters reflecting glucose fluctuation and decreased insulin secretory capacity in patients with T2DM. Further longitudinal, prospective studies are needed to investigate a causal relationship between glucose fluctuations, renal tubular damage, and other vascular complications of diabetes.",
author = "Kim, {So Ra} and Lee, {Yong Ho} and Lee, {Sang Guk} and Kang, {Eun Seok} and Cha, {Bong Soo} and Kim, {Jeong Ho} and byungwan lee",
year = "2016",
month = "7",
day = "1",
doi = "10.1097/MD.0000000000004114",
language = "English",
volume = "95",
journal = "Medicine (United States)",
issn = "0025-7974",
publisher = "Lippincott Williams and Wilkins",
number = "27",

}

Urinary N -acetyl-β- d -glucosaminidase, an early marker of diabetic kidney disease, might reflect glucose excursion in patients with type 2 diabetes. / Kim, So Ra; Lee, Yong Ho; Lee, Sang Guk; Kang, Eun Seok; Cha, Bong Soo; Kim, Jeong Ho; lee, byungwan.

In: Medicine (United States), Vol. 95, No. 27, e4114, 01.07.2016.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Urinary N -acetyl-β- d -glucosaminidase, an early marker of diabetic kidney disease, might reflect glucose excursion in patients with type 2 diabetes

AU - Kim, So Ra

AU - Lee, Yong Ho

AU - Lee, Sang Guk

AU - Kang, Eun Seok

AU - Cha, Bong Soo

AU - Kim, Jeong Ho

AU - lee, byungwan

PY - 2016/7/1

Y1 - 2016/7/1

N2 - Recently, several renal tubular damage markers have gained considerable attention because of their clinical implications as sensitive and specific biomarkers for early stage diabetic kidney disease. However, little is known about the demographic and glucometabolic factors affecting levels of urinary N-acetyl-β-d-glucosaminidase (NAG), a marker of proximal tubular damage, in type 2 diabetes mellitus (T2DM). The aim of this study was to investigate the clinical relevance of urinary NAG with regard to demographic and glucometabolic parameters, as well as nephropathic parameters, by comparing the glomerulopathic marker of albuminuria. In this retrospective cross-sectional study, we enrolled a total of 592 patients with either prediabetes (N = 29) or T2DM (N = 563). Glucometabolic parameters (glucose, hemoglobin A1c, glycated albumin [GA], insulin, C-peptide, homeostasis model assessment [HOMA] of insulin resistance, HOMA-β, postprandial C-peptide-to-glucose ratio [PCGR], and urinary glucose-to-creatinine ratio) and nephropathic parameters (urinary NAG, albumin-to-creatinine ratio [ACR], and estimated glomerular filtration rate) were measured. The levels of urinary NAG showed moderate positive correlation with the levels of urinary ACR in T2DM (r = 0.46). In correlation analysis, urinary NAG was more strongly correlated with body mass index (BMI) (r = -0.22; P < 0.001 vs. r = -0.02; P = 0.74), plasma stimulated glucose (r = 0.25; P < 0.001 vs. r = 0.08; P = 0.10), GA (r = 0.20; P < 0.001 vs. r = 0.13; P = 0.01), PCGR (r = -0.17; P = 0.001 vs. r = -0.09; P = 0.11), and HOMA-β (r = -0.10; P = 0.05 vs. r = -0.02; P = 0.79) than urinary ACR. In multiple regression analysis, age, lower BMI, stimulated glucose, GA, and urinary ACR predicted increased urinary NAG. In conclusion, increase in urinary NAG may be related to glycemic parameters reflecting glucose fluctuation and decreased insulin secretory capacity in patients with T2DM. Further longitudinal, prospective studies are needed to investigate a causal relationship between glucose fluctuations, renal tubular damage, and other vascular complications of diabetes.

AB - Recently, several renal tubular damage markers have gained considerable attention because of their clinical implications as sensitive and specific biomarkers for early stage diabetic kidney disease. However, little is known about the demographic and glucometabolic factors affecting levels of urinary N-acetyl-β-d-glucosaminidase (NAG), a marker of proximal tubular damage, in type 2 diabetes mellitus (T2DM). The aim of this study was to investigate the clinical relevance of urinary NAG with regard to demographic and glucometabolic parameters, as well as nephropathic parameters, by comparing the glomerulopathic marker of albuminuria. In this retrospective cross-sectional study, we enrolled a total of 592 patients with either prediabetes (N = 29) or T2DM (N = 563). Glucometabolic parameters (glucose, hemoglobin A1c, glycated albumin [GA], insulin, C-peptide, homeostasis model assessment [HOMA] of insulin resistance, HOMA-β, postprandial C-peptide-to-glucose ratio [PCGR], and urinary glucose-to-creatinine ratio) and nephropathic parameters (urinary NAG, albumin-to-creatinine ratio [ACR], and estimated glomerular filtration rate) were measured. The levels of urinary NAG showed moderate positive correlation with the levels of urinary ACR in T2DM (r = 0.46). In correlation analysis, urinary NAG was more strongly correlated with body mass index (BMI) (r = -0.22; P < 0.001 vs. r = -0.02; P = 0.74), plasma stimulated glucose (r = 0.25; P < 0.001 vs. r = 0.08; P = 0.10), GA (r = 0.20; P < 0.001 vs. r = 0.13; P = 0.01), PCGR (r = -0.17; P = 0.001 vs. r = -0.09; P = 0.11), and HOMA-β (r = -0.10; P = 0.05 vs. r = -0.02; P = 0.79) than urinary ACR. In multiple regression analysis, age, lower BMI, stimulated glucose, GA, and urinary ACR predicted increased urinary NAG. In conclusion, increase in urinary NAG may be related to glycemic parameters reflecting glucose fluctuation and decreased insulin secretory capacity in patients with T2DM. Further longitudinal, prospective studies are needed to investigate a causal relationship between glucose fluctuations, renal tubular damage, and other vascular complications of diabetes.

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