title: Splenectomy protects the kidneys against ischemic reperfusion injury in the rat.
abstract: BACKGROUND
  Ischemic reperfusion (I/R) injury of the kidney is closely associated with delayed graft function, increased acute rejection, and late allograft dysfunction. Splenectomy reduced hepatic I/R injury by inhibiting leukocyte infiltration in the liver, release of TNF-α, cell apoptosis, and expression of caspase-3. Thus, we investigated the effects of splenectomy on renal I/R injury in the rat.
  
  
  METHODS
  Male Wistar rats were assigned to four groups: sham operation (sham group), sham operation+splenectomy (sham+SPLN group), right nephrectomy followed by clamping the left renal pedicle for 30min (I/R 30 group), and I/R 30+splenectomy (I/R 30+SPLN group). Renal function was determined by measuring the concentration of blood urea nitrogen (BUN) and serum creatinine (S-Cr). The serum level of tumor necrosis factor-α (TNF-α) was measured as the marker for inflammation. Left kidneys were obtained 24h after reperfusion. TUNEL assay was assessed for cell apoptosis. Spleens were obtained immediately (0-h group) and 3h after reperfusion (3-h group). The removed spleens were histologically evaluated.
  
  
  RESULTS
  The BUN and S-Cr levels were significantly lower in the I/R 30+SPLN group than in the I/R 30 group (p<0.05 for both). Apoptotic cells were significantly lower in the I/R 30+SPLN group than in the I/R 30 group. The serum level of TNF-α, which was increased after I/R, was significantly lower in the I/R 30+SPLN group than in the I/R 30 group (p<0.05). Spleen weights were significantly lower in the 3-h group than in the 0-h group (p<0.05).
  
  
  CONCLUSIONS
  These results suggest that splenectomy reduces renal I/R injury, and this effect may occur by an anti-inflammatory pathway and inhibition of cell apoptosis.
authors.affiliation: Department of Urology, Graduate School of Medicine, Yamaguchi University,Yamaguchi, Japan. k012um@yamaguchi-u.ac.jp
authors.forename: Toshiya
authors.initials: T
authors.lastname: Hiroyoshi
authors.forename: Masahiro
authors.initials: M
authors.lastname: Tsuchida
authors.forename: Koichi
authors.initials: K
authors.lastname: Uchiyama
authors.forename: Koki
authors.initials: K
authors.lastname: Fujikawa
authors.forename: Takahiro
authors.initials: T
authors.lastname: Komatsu
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Kanaoka
authors.forename: Hideyasu
authors.initials: H
authors.lastname: Matsuyama
mesh_terms: D000818:Animals; D017209:Apoptosis; D001806:Blood Urea Nitrogen; D053148:Caspase 3 / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D007249:Inflammation / Q000276:immunology; D007668:Kidney / Q000473:pathology*; D008099:Liver / Q000473:pathology; D008297:Male; D009392:Nephrectomy; D009929:Organ Size; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000517:prevention & control*; D013156:Splenectomy; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D014409:Tumor Necrosis Factor-alpha; D003404:Creatinine; D053148:Caspase 3