PMID- 30712924
OWN - NLM
STAT- In-Process
LR  - 20190725
IS  - 1523-1755 (Electronic)
IS  - 0085-2538 (Linking)
VI  - 95
IP  - 3
DP  - 2019 Mar
TI  - Urinary levels of the leukocyte surface molecule CD11b associate with glomerular 
      inflammation in lupus nephritis.
PG  - 680-692
LID - S0085-2538(18)30826-3 [pii]
LID - 10.1016/j.kint.2018.10.025 [doi]
AB  - Noninvasive biomarkers of disease activity are needed to monitor response to
      therapy and predict disease recurrence in patients with glomerulonephritis. The
      leukocyte surface markers integrin Mac-1 and CD16b have been implicated in the
      pathogenesis of lupus nephritis (LN). Mac-1 comprises a unique alpha subunit
      (CD11b) complexed with a common beta2 subunit, which are released along with
      CD16b from specific leukocyte subsets under inflammatory conditions including
      glomerulonephritis. We investigated the association of urinary CD11b and CD16b
      with histopathological activity in 272 patients with biopsy-proven glomerular
      diseases, including 118 with LN. Urine CD11b and CD16b were measured via
      enzyme-linked immunosorbent assay. Urinary levels of both markers were increased 
      in LN, but only urinary CD11b was correlated with the number of glomerular
      leukocytes and with overall histopathological activity. In a subset of patients
      with samples available from the time of biopsy and subsequent clinical remission 
      of LN, urinary levels of CD11b decreased with successful glucocorticoid
      treatment. Receiver-operating characteristic curve analysis demonstrated that
      urinary CD11b was superior to CD16b, the scavenger receptor CD163, and monocyte
      chemotactic protein-1 for the prediction of proliferative LN. In anti-mouse
      nephrotoxic serum glomerulonephritis, urinary CD11b correlated with histologic
      damage and decreased with corticosteroid treatment. In vitro, CD11b levels were
      decreased on activated mouse neutrophils displaying Fcgamma receptor clustering
      and transendothelial migration, suggesting that leukocyte activation and
      transmigration are required for CD11b shedding in urine. Together, our results
      suggest that urinary CD11b may be a useful biomarker to estimate
      histopathological activity, particularly glomerular leukocyte accumulation, in
      LN.
CI  - Copyright (c) 2019 International Society of Nephrology. Published by Elsevier
      Inc. All rights reserved.
FAU - Kitagawa, Akimitsu
AU  - Kitagawa A
AD  - Department of Nephrology, Internal Medicine, Nagoya University Graduate School of
      Medicine, Nagoya, Aichi, Japan.
FAU - Tsuboi, Naotake
AU  - Tsuboi N
AD  - Department of Nephrology, Internal Medicine, Nagoya University Graduate School of
      Medicine, Nagoya, Aichi, Japan; Department of Nephrology, School of Medicine,
      Fujita Health University, Toyoake, Aichi, Japan. Electronic address:
      nao-take@fujita-hu.ac.jp.
FAU - Yokoe, Yuki
AU  - Yokoe Y
AD  - Department of Nephrology, Internal Medicine, Nagoya University Graduate School of
      Medicine, Nagoya, Aichi, Japan.
FAU - Katsuno, Takayuki
AU  - Katsuno T
AD  - Department of Nephrology and Rheumatology, Aichi Medical University, Nagakute,
      Aichi, Japan.
FAU - Ikeuchi, Hidekazu
AU  - Ikeuchi H
AD  - Department of Nephrology and Rheumatology, Gunma University Graduate School of
      Medicine, Maebashi, Gunma, Japan.
FAU - Kajiyama, Hiroshi
AU  - Kajiyama H
AD  - Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama
      Medical University, Iruma, Saitama, Japan.
FAU - Endo, Nobuhide
AU  - Endo N
AD  - Department of Nephrology, Internal Medicine, Nagoya University Graduate School of
      Medicine, Nagoya, Aichi, Japan.
FAU - Sawa, Yuriko
AU  - Sawa Y
AD  - Department of Nephrology, Internal Medicine, Nagoya University Graduate School of
      Medicine, Nagoya, Aichi, Japan.
FAU - Suwa, Junya
AU  - Suwa J
AD  - Department of Nephrology and Rheumatology, Gunma University Graduate School of
      Medicine, Maebashi, Gunma, Japan.
FAU - Sugiyama, Yutaka
AU  - Sugiyama Y
AD  - Department of Nephrology, Internal Medicine, Nagoya University Graduate School of
      Medicine, Nagoya, Aichi, Japan.
FAU - Hachiya, Asaka
AU  - Hachiya A
AD  - Department of Nephrology, Internal Medicine, Nagoya University Graduate School of
      Medicine, Nagoya, Aichi, Japan.
FAU - Mimura, Toshihide
AU  - Mimura T
AD  - Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama
      Medical University, Iruma, Saitama, Japan.
FAU - Hiromura, Keiju
AU  - Hiromura K
AD  - Department of Nephrology and Rheumatology, Gunma University Graduate School of
      Medicine, Maebashi, Gunma, Japan.
FAU - Maruyama, Shoichi
AU  - Maruyama S
AD  - Department of Nephrology, Internal Medicine, Nagoya University Graduate School of
      Medicine, Nagoya, Aichi, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190131
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
SB  - IM
OTO - NOTNLM
OT  - *glomerulonephritis
OT  - *inflammation
OT  - *kidney biopsy
OT  - *lupus
OT  - *macrophages
EDAT- 2019/02/05 06:00
MHDA- 2019/02/05 06:00
CRDT- 2019/02/05 06:00
PHST- 2018/03/14 00:00 [received]
PHST- 2018/10/01 00:00 [revised]
PHST- 2018/10/18 00:00 [accepted]
PHST- 2019/02/05 06:00 [pubmed]
PHST- 2019/02/05 06:00 [medline]
PHST- 2019/02/05 06:00 [entrez]
AID - S0085-2538(18)30826-3 [pii]
AID - 10.1016/j.kint.2018.10.025 [doi]
PST - ppublish
SO  - Kidney Int. 2019 Mar;95(3):680-692. doi: 10.1016/j.kint.2018.10.025. Epub 2019
      Jan 31.