PMID- 27399115
OWN - NLM
STAT- MEDLINE
DCOM- 20170221
LR  - 20231111
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 95
IP  - 27
DP  - 2016 Jul
TI  - Urinary N-acetyl-beta-D-glucosaminidase, an early marker of diabetic kidney disease, 
      might reflect glucose excursion in patients with type 2 diabetes.
PG  - e4114
LID - 10.1097/MD.0000000000004114 [doi]
LID - e4114
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-beta-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-beta, 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-beta (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.
FAU - Kim, So Ra
AU  - Kim SR
AD  - Division of Endocrinology and Metabolism, Department of Internal Medicine, 
      Graduate School, Yonsei University College of Medicine Severance Hospital 
      Department of Laboratory Medicine, Yonsei University College of Medicine, Seoul, 
      Republic of Korea.
FAU - Lee, Yong-Ho
AU  - Lee YH
FAU - Lee, Sang-Guk
AU  - Lee SG
FAU - Kang, Eun Seok
AU  - Kang ES
FAU - Cha, Bong-Soo
AU  - Cha BS
FAU - Kim, Jeong-Ho
AU  - Kim JH
FAU - Lee, Byung-Wan
AU  - Lee BW
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Biomarkers)
RN  - EC 3.2.1.52 (Acetylglucosaminidase)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Acetylglucosaminidase/*urine
MH  - Aged
MH  - Albuminuria/urine
MH  - Biomarkers/urine
MH  - Cross-Sectional Studies
MH  - Diabetes Mellitus, Type 2/*metabolism/*urine
MH  - Diabetic Nephropathies/*diagnosis/*urine
MH  - Female
MH  - Glucose/*metabolism
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Time Factors
PMC - PMC5058844
COIS- The authors have no conflicts of interest to disclose.
EDAT- 2016/07/12 06:00
MHDA- 2017/02/22 06:00
PMCR- 2016/07/08
CRDT- 2016/07/12 06:00
PHST- 2016/07/12 06:00 [entrez]
PHST- 2016/07/12 06:00 [pubmed]
PHST- 2017/02/22 06:00 [medline]
PHST- 2016/07/08 00:00 [pmc-release]
AID - 00005792-201607050-00059 [pii]
AID - 10.1097/MD.0000000000004114 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2016 Jul;95(27):e4114. doi: 10.1097/MD.0000000000004114.