PubTransformer

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PMID- 28864372
OWN - NLM
STAT- MEDLINE
DA  - 20170902
DCOM- 20170908
LR  - 20170908
IS  - 1538-2990 (Electronic)
IS  - 0002-9629 (Linking)
VI  - 354
IP  - 2
DP  - 2017 Aug
TI  - Therapeutic Mechanism of Glucocorticoids on Cellular Crescent Formation in
      Patients With Antiglomerular Basement Membrane Disease.
PG  - 145-151
LID - S0002-9629(17)30227-6 [pii]
LID - 10.1016/j.amjms.2017.04.015 [doi]
AB  - BACKGROUND: This study aimed to explore the therapeutic mechanism of
      glucocorticoids (GCs) in antiglomerular basement membrane disease. MATERIALS AND 
      METHODS: Thirty-four patients with biopsy-proven antiglomerular basement membrane
      nephritis were divided into the following 2 groups: group 1 (patients treated
      with GCs, n = 22) and group 2 (patients who were not treated with GCs, n = 12).
      The expression of parietal epithelial cells (PECs), activated PECs and
      glucocorticoid receptors (GRs) was examined quantitatively and compared between
      the 2 groups. Correlations between GR expression in glomeruli and patients'
      clinicopathological indices were also analyzed. RESULTS: Compared with patients
      in group 2, patients in group 1 showed lower levels of serum creatinine (SCr) (P 
      = 0.03), average cellular crescent percentage (P = 0.005) and macrophages
      infiltrating in renal interstitium (P = 0.03). PECs (P = 0.007) and activated
      PECs (P = 0.03) were strongly detected in the cellular components of classic
      crescents, and both were significantly reduced in group 1 compared to group 2. GR
      expression either in glomeruli (P = 0.01) or interstitium (P = 0.009) was lower
      in group 1 after GCs treatment than in group 2. Additionally, GR expression in
      glomeruli was strongly correlated with renal function (SCr: r = 0.45, P = 0.009; 
      eGFR: r = -0.35, P = 0.046), the proportion of cellular crescents (r = 0.67, P < 
      0.001), PECs (r = 0.64, P < 0.001) and activated PECs (r = 0.72, P < 0.001), and 
      the degree of interstitial (r = 0.50, P = 0.004) and glomerular (r = 0.49, P =
      0.007) macrophage infiltration. CONCLUSIONS: GCs might exert their therapeutic
      effects via inhibiting the activation and proliferation of PECs, as well as
      macrophage infiltration, which could contribute to crescent formation and
      determine renal survival. GRs are involved in this process as well.
CI  - Copyright (c) 2017 Southern Society for Clinical Investigation. Published by
      Elsevier Inc. All rights reserved.
FAU - Wu, Xiaomei
AU  - Wu X
AD  - National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing
      University School of Medicine, Nanjing, China.
FAU - Zhang, Mingchao
AU  - Zhang M
AD  - National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing
      University School of Medicine, Nanjing, China.
FAU - Huang, Xiao
AU  - Huang X
AD  - National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing
      University School of Medicine, Nanjing, China.
FAU - Zhang, Lihua
AU  - Zhang L
AD  - National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing
      University School of Medicine, Nanjing, China.
FAU - Zeng, Caihong
AU  - Zeng C
AD  - National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing
      University School of Medicine, Nanjing, China.
FAU - Zhang, Jiong
AU  - Zhang J
AD  - National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing
      University School of Medicine, Nanjing, China. Electronic address:
      [email protected]
FAU - Liu, Zhihong
AU  - Liu Z
AD  - National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing
      University School of Medicine, Nanjing, China.
FAU - Tang, Zheng
AU  - Tang Z
AD  - National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing
      University School of Medicine, Nanjing, China. Electronic address:
      [email protected]
LA  - eng
PT  - Journal Article
DEP - 20170425
PL  - United States
TA  - Am J Med Sci
JT  - The American journal of the medical sciences
JID - 0370506
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Glucocorticoids)
RN  - 0 (Receptors, Glucocorticoid)
SB  - AIM
SB  - IM
MH  - Adult
MH  - Anti-Glomerular Basement Membrane Disease/drug therapy/metabolism/*pathology
MH  - Anti-Inflammatory Agents/pharmacology/therapeutic use
MH  - China
MH  - Epithelial Cells/drug effects
MH  - Female
MH  - Glucocorticoids/metabolism/*pharmacology/therapeutic use
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Receptors, Glucocorticoid/*genetics/metabolism
MH  - Young Adult
OTO - NOTNLM
OT  - Activation and proliferation
OT  - Crescent
OT  - Glucocorticoid receptor
OT  - Glucocorticoids
OT  - Parietal epithelial cells
EDAT- 2017/09/03 06:00
MHDA- 2017/09/09 06:00
CRDT- 2017/09/03 06:00
PHST- 2017/03/03 [received]
PHST- 2017/04/07 [revised]
PHST- 2017/04/20 [accepted]
AID - S0002-9629(17)30227-6 [pii]
AID - 10.1016/j.amjms.2017.04.015 [doi]
PST - ppublish
SO  - Am J Med Sci. 2017 Aug;354(2):145-151. doi: 10.1016/j.amjms.2017.04.015. Epub
      2017 Apr 25.