PMID- 27279796
OWN - NLM
STAT- MEDLINE
DCOM- 20170417
LR  - 20220317
IS  - 1449-1907 (Electronic)
IS  - 1449-1907 (Linking)
VI  - 13
IP  - 6
DP  - 2016
TI  - Differential microRNA Profiles Predict Diabetic Nephropathy Progression in 
      Taiwan.
PG  - 457-65
LID - 10.7150/ijms.15548 [doi]
AB  - OBJECTIVES: Diabetic nephropathy (DN) is a major leading cause of kidney failure. 
      Recent studies showed that serological microRNAs (miRs) could be utilized as 
      biomarkers to identify disease pathogenesis; the DN-related miRs, however, 
      remained to be explored. METHODS: A prospective case-control study was conducted. 
      The clinical significance of five potential miRs (miR-21, miR-29a, miR-29b, 
      miR-29c and miR192) in type 2 Diabetes Mellitus (T2DM) patients who have existing 
      diabetic retinopathy with differential Albumin:Creatinine Ratio (ACR) and 
      estimated Glomerular Filtration Rate (eGFR) was performed using quantitative 
      RT-PCR analysis. The subjects with diabetic retinopathy enrolled in Taipei City 
      Hospital, Taiwan, were classified into groups of normal albuminuria (ACR<30mg/g; 
      N=12); microalbuminuria (30mg/g<ACR<300mg/g; N=17) and overt proteinuria 
      (ACR>300mg/g; N=21) as well as 18 low-eGFR (eGFR<60ml/min) and 32 high-eGFR 
      (eGFR>60ml/min). The level of serum miRs was statistically correlated with age, 
      Glucose AC, ACR, eGFR and DN progression. RESULTS: The levels of miR-21, miR-29a 
      and miR-192 were significantly enriched in the overt proteinuria group compared 
      with microalbuminuria and/or overt proteinuria groups. It was shown that only 
      miR-21 level was significantly up-regulated in low-eGFR group compared with 
      high-eGFR patients. Interestingly, Pearson's correlation coefficient analysis 
      demonstrated that DN progressors showed significantly greater levels of miR-21, 
      miR-29a, miR-29b and miR-29c in comparison with non-progressors implying the 
      clinical potential of DN associated miRs in monitoring and preventing disease 
      advancement. CONCLUSION: Our findings showed that miR-21, miR-29a/b/c and miR-192 
      could reflect DN pathogenesis and serve as biomarkers during DN progression.
FAU - Chien, Hung-Yu
AU  - Chien HY
AD  - 1. Department of Endocrinology & Metabolism, Taipei City Hospital, Ren-Ai Branch, 
      Taipei, Taiwan;
FAU - Chen, Chang-Yi
AU  - Chen CY
AD  - 2. Institute of Oral Biology and Department of Dentistry, School of Dentistry, 
      National Yang-Ming University, Taipei, Taiwan;
FAU - Chiu, Yen-Hui
AU  - Chiu YH
AD  - 3. Department of Education and Research, Taipei City Hospital, Taipei, Taiwan;
FAU - Lin, Yi-Chun
AU  - Lin YC
AD  - 4. Division of Endocrinology &Metabolism, Taipei Veterans General Hospital, 
      Taipei, Taiwan;; 5. Faculty of Medicine, National Yang-Ming University, Taipei, 
      Taiwan;
FAU - Li, Wan-Chun
AU  - Li WC
AD  - 2. Institute of Oral Biology and Department of Dentistry, School of Dentistry, 
      National Yang-Ming University, Taipei, Taiwan;; 3. Department of Education and 
      Research, Taipei City Hospital, Taipei, Taiwan;
LA  - eng
PT  - Journal Article
DEP - 20160601
PL  - Australia
TA  - Int J Med Sci
JT  - International journal of medical sciences
JID - 101213954
RN  - 0 (Biomarkers)
RN  - 0 (MIRN21 microRNA, human)
RN  - 0 (MIRN29a microRNA, human)
RN  - 0 (MicroRNAs)
RN  - AYI8EX34EU (Creatinine)
SB  - IM
MH  - Albuminuria/blood
MH  - Biomarkers/blood
MH  - Case-Control Studies
MH  - Creatinine/blood
MH  - Diabetes Mellitus, Type 2/blood/genetics
MH  - Diabetic Nephropathies/blood/*genetics
MH  - Disease Progression
MH  - Glomerular Filtration Rate/physiology
MH  - Humans
MH  - MicroRNAs/*genetics
MH  - Prospective Studies
MH  - Risk Factors
MH  - Taiwan
PMC - PMC4893561
OTO - NOTNLM
OT  - Albumin:creatinine ratio
OT  - Biomarkers
OT  - Circulating microRNA
OT  - Diabetic nephropathy
OT  - Estimated Glomerular Filtration Rate.
COIS- Competing interests: The authors declare no competing interest exists.
EDAT- 2016/06/10 06:00
MHDA- 2017/04/18 06:00
PMCR- 2016/01/01
CRDT- 2016/06/10 06:00
PHST- 2016/03/15 00:00 [received]
PHST- 2016/05/09 00:00 [accepted]
PHST- 2016/06/10 06:00 [entrez]
PHST- 2016/06/10 06:00 [pubmed]
PHST- 2017/04/18 06:00 [medline]
PHST- 2016/01/01 00:00 [pmc-release]
AID - ijmsv13p0457 [pii]
AID - 10.7150/ijms.15548 [doi]
PST - epublish
SO  - Int J Med Sci. 2016 Jun 1;13(6):457-65. doi: 10.7150/ijms.15548. eCollection 
      2016.