PMID- 7565482
OWN - NLM
STAT- MEDLINE
DCOM- 19951114
LR  - 20051116
IS  - 0378-0392 (Print)
IS  - 0378-0392 (Linking)
VI  - 21
IP  - 4-5
DP  - 1995
TI  - Tumor necrosis factor in renal injury.
PG  - 336-41
AB  - Inflammatory diseases of the renal glomerulus and tubulointerstitium are 
      characterized by destructive and restorative processes. These alterations are 
      mediated by soluble molecules, including cytokines that instruct target cells to 
      alter their proliferation, differentiation phenotype, secretion and migration. 
      One of these cytokines is tumor necrosis factor-alpha (TNF alpha). Its expression 
      within the glomerulus has been observed in both resident cells and infiltrating 
      monocytes/macrophages in response to cell stimulation with chemicals, immune 
      complexes, bacterial lipopolysaccharides, and advanced glycosylation end 
      products. Its release can be amplified by deposits of terminal complement 
      proteins (C5b-9) or formation of platelet-activating factor and reactive oxygen 
      species, and, on the contrary, blunted by that of prostaglandins or 
      anti-inflammatory interleukin (IL)-6 and IL-10. The roles of TNF alpha in the 
      pathogenesis of glomerular diseases include reduction of blood flow and 
      filtration rate, alteration of the barrier function of capillary wall, formation 
      of capillary thrombi and infiltration of the structure by blood-borne cells. 
      Expression of TNF alpha has been observed in tubulointerstitium as well, mainly 
      in proximal tubular epithelial cells. In vitro, this expression can be amplified 
      by IL-1 and, inversely, suppressed by immunosuppressive drugs. Roles of TNF alpha 
      in tubulointerstitium remain largely undefined, but may include infiltration of 
      the interstitium by inflammatory cells and alteration in tubular transport of 
      fluid and electrolytes. Extensive study will be necessary to further elucidate 
      intracellular signals induced by TNF alpha binding to target cells within the 
      kidney and thus to establish possibilities of therapeutic intervention.
FAU - Baud, L
AU  - Baud L
AD  - INSERM U.64, Hopital Tenon, Paris, France.
FAU - Ardaillou, R
AU  - Ardaillou R
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Switzerland
TA  - Miner Electrolyte Metab
JT  - Mineral and electrolyte metabolism
JID - 7802196
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Glomerulonephritis/*etiology
MH  - Humans
MH  - Nephritis, Interstitial/*etiology
MH  - Tumor Necrosis Factor-alpha/*physiology
RF  - 55
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PST - ppublish
SO  - Miner Electrolyte Metab. 1995;21(4-5):336-41.