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Tumor necrosis factor‐alpha response to shock wave lithotripsy‐induced renal injury
Author(s) -
Clark Daniel Lynn,
Handa R. K.,
Johnson C. D.,
Connors B. A.,
Evan A. P.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1160.7
Subject(s) - tumor necrosis factor alpha , medicine , kidney , urinary system , inflammation , urology , necrosis , saline , lithotripsy , urine , shock wave lithotripsy , endocrinology , surgery
Shock wave lithotripsy (SWL) induces a rapid inflammatory response in renal tissue. This study investigated the site of the inflammatory response in a porcine model of acute SWL‐induced renal injury, using tumor necrosis factor alpha (TNF) as a marker of inflammation. The lower pole left renal calyx of anesthetized female pigs (30–35 lbs) received 2000 shock waves (SW) from a Dornier HM3 lithotripter (24 kV, 120 SW/min). Blood and urine samples were taken at timed intervals. At 4 hours post‐treatment, kidneys were perfused with cold saline, excised, and tissue samples were flash‐frozen in liquid N2. TNF was measured by ELISA (BioSource). Left urinary TNF excretion peaked by 1 hr post‐SWL (23.8±20.9 pg/min vs. 0.0±0.0 pg/min for control, p<0.001) and although declining remained significantly elevated up to 4 hrs post‐SWL. Right urinary TNF excretion, renal tissue TNF, and plasma TNF levels were unchanged after SWL. These data correlate with our previously reported IL‐6 and currently observed HO‐1 data suggesting that inflammation and oxidative stress are primarily occurring in the shocked kidney. Supported by NIH grant DK67133.