PMID- 8725616
OWN - NLM
STAT- MEDLINE
DCOM- 19961121
LR  - 20190830
IS  - 0160-564X (Print)
IS  - 0160-564X (Linking)
VI  - 20
IP  - 5
DP  - 1996 May
TI  - Soluble TNF alpha receptors are increased in chronic renal insufficiency and 
      hemodialysis and inhibit neutrophil priming by TNF alpha.
PG  - 390-5
AB  - The oxidative burst of neutrophils from azotemic patients is refractory to 
      priming by tumor necrosis factor-alpha (TNF alpha). Soluble TNF alpha binding 
      protiens (sTNFR) accumulate in the plasma of azotemic patients. To test the 
      hypothesis that these increased sTNFR concentrations inhibit TNF alpha priming of 
      oxidative burst activity, we measured plasma sTNFR concentrations in nondialyzed 
      azotemic patients, hemodialysis patients, and normal subjects, and determined TNF 
      alpha priming of fMet-Leu-Phe-stimulated superoxide production in neutrophils 
      incubated in plasma with differing levels of sT-NFR. These sTNFR concentrations 
      increased significantly as creatinine clearance decreased and were significantly 
      greater in hemodialysis patients than could be accounted for by loss of renal 
      function alone. TNF alpha primed superoxide production by normal neutrophils in 
      normal plasma, but this effect was significantly reduced in plasma with increased 
      concentrations of sTNFR. Neutrophils from azotemic and hemodialysis patients were 
      refractory to priming by TNF alpha in autologous plasma, and incubation in normal 
      plasma only partially corrected this defect. We conclude that sTNFR accumulate as 
      a result of the loss of renal function and hemodialysis and inhibit TNF alpha 
      priming of neutrophils in azotemic and hemodialysis patients, but that these 
      cells also have an intrinsic functional defect.
FAU - Ward, R
AU  - Ward R
AD  - Department of Medicine, School of Medicine, University of Louisville, Kentucky 
      40292, USA.
FAU - McLeish, K R
AU  - McLeish KR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Artif Organs
JT  - Artificial organs
JID - 7802778
RN  - 0 (Antigens, CD)
RN  - 0 (Blood Proteins)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 11062-77-4 (Superoxides)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antigens, CD/blood/*metabolism
MH  - Blood Proteins/metabolism
MH  - Female
MH  - Humans
MH  - Kidney Failure, Chronic/*metabolism
MH  - Male
MH  - Middle Aged
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - Neutrophils/drug effects/*metabolism
MH  - Protein Binding
MH  - Receptors, Tumor Necrosis Factor/blood/*metabolism
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Regression Analysis
MH  - *Renal Dialysis
MH  - Respiratory Burst
MH  - Superoxides/metabolism
MH  - Tumor Necrosis Factor-alpha/*metabolism
MH  - Uremia/blood/therapy
EDAT- 1996/05/01 00:00
MHDA- 1996/05/01 00:01
CRDT- 1996/05/01 00:00
PHST- 1996/05/01 00:00 [pubmed]
PHST- 1996/05/01 00:01 [medline]
PHST- 1996/05/01 00:00 [entrez]
AID - 10.1111/j.1525-1594.1996.tb04521.x [doi]
PST - ppublish
SO  - Artif Organs. 1996 May;20(5):390-5. doi: 10.1111/j.1525-1594.1996.tb04521.x.