PMID- 27603798
OWN - NLM
STAT- MEDLINE
DCOM- 20180109
LR  - 20180906
IS  - 1421-9670 (Electronic)
IS  - 0250-8095 (Linking)
VI  - 44
IP  - 4
DP  - 2016
TI  - Early Changes in Monocyte Adhesion Molecule Expression and Tumor Necrosis 
      Factor-alpha Levels in Chronic Kidney Disease - A 5-Year Prospective Study.
PG  - 268-275
AB  - BACKGROUND: Despite the absence of clinical symptoms, patients with chronic 
      kidney disease (CKD) exhibit elevated levels of pro-inflammatory markers. To 
      investigate whether it is possible to detect inflammatory activity and altered 
      monocyte function at an early stage of renal disease, we studied patients with 
      CKD stages 2-3 over 5 years. METHODS: The expression of adhesion molecules on 
      monocytes at resting state and after stimulation with 
      formyl-methionyl-leucyl-phenylalanine (fMLP), as well as oxidative metabolism 
      capacity was measured with flow cytometry in 108 CKD patients and healthy 
      controls. Soluble markers of inflammation, such as cytokines, were analyzed using 
      the Milliplex technique. RESULTS: Patients showed significantly lower CD11b 
      expression after stimulation during the 3rd (p = 0.002) and the 5th year (p < 
      0.001), together with a lower oxidative burst in response to fMLP over time (p = 
      0.02). The expression of CD62L on resting monocytes was lower during the 3rd (p = 
      0.001) and the 5th (p = 0.001) year in patients. Levels of tumor necrosis 
      factor-alpha and RANTES were significantly increased (p = 0.001, p = 0.006) and 
      interleukin-12 levels were also higher in CKD patients during the 5th year (p = 
      0.007). CONCLUSION: Monocytes in CKD stages 2-3 show emerging functional 
      abrasions, with altered adhesion molecule expression and impaired fMLP response. 
      These findings suggest that a transformation of monocyte function occurs at an 
      early phase of renal impairment and may together with increased plasma levels of 
      pro-inflammatory cytokines contribute to the higher vulnerability of CKD patients 
      to comorbidities, such as infections and cardiovascular disease.
CI  - (c) 2016 S. Karger AG, Basel.
FAU - Wallquist, Carin
AU  - Wallquist C
AD  - Department of Nephrology, Karolinska Institutet, and Karolinska University 
      Hospital, Stockholm, Sweden.
FAU - Mansouri, Ladan
AU  - Mansouri L
FAU - Norrback, Mattias
AU  - Norrback M
FAU - Hylander, Britta
AU  - Hylander B
FAU - Jacobson, Stefan H
AU  - Jacobson SH
FAU - Lundahl, Joachim
AU  - Lundahl J
LA  - eng
PT  - Journal Article
DEP - 20160908
PL  - Switzerland
TA  - Am J Nephrol
JT  - American journal of nephrology
JID - 8109361
RN  - 0 (CD11b Antigen)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126880-86-2 (L-Selectin)
RN  - 187348-17-0 (Interleukin-12)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
SB  - IM
MH  - Adult
MH  - CD11b Antigen/*blood
MH  - Case-Control Studies
MH  - Cells, Cultured
MH  - Chemokine CCL5/blood
MH  - Female
MH  - Humans
MH  - Interleukin-12/blood
MH  - L-Selectin/*blood
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Monocytes/drug effects/*metabolism/physiology
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - Prospective Studies
MH  - Renal Insufficiency, Chronic/*blood
MH  - Respiratory Burst/drug effects
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*blood
EDAT- 2016/10/19 06:00
MHDA- 2018/01/10 06:00
CRDT- 2016/09/08 06:00
PHST- 2016/05/16 00:00 [received]
PHST- 2016/08/10 00:00 [accepted]
PHST- 2016/10/19 06:00 [pubmed]
PHST- 2018/01/10 06:00 [medline]
PHST- 2016/09/08 06:00 [entrez]
AID - 000449290 [pii]
AID - 10.1159/000449290 [doi]
PST - ppublish
SO  - Am J Nephrol. 2016;44(4):268-275. doi: 10.1159/000449290. Epub 2016 Sep 8.