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-dependent bilateral renal injury is induced by
unilateral renal ischemia-reperfusion
Department of Urology, Johns Hopkins University, Baltimore, Maryland 21287; and Department of Surgery, University of Colorado Health Sciences Center, Denver, Colorado 80262
While tumor necrosis factor
(TNF)-
is an important mediator of renal
ischemia-reperfusion (I/R) injury, its role in contralateral renal injury after isolated renal ischemia remains unknown. We therefore investigated the effect of isolated left renal
ischemia on the nonischemic contralateral kidney.
To study this, male Sprague-Dawley rats were anesthetized and exposed
to varying degrees of left renal I/R injury. Both kidneys were
subsequently harvested, serum samples were obtained, and TNF-
protein expression (ELISA), TNF- mRNA content (RT-PCR), TNF-
immunolocalization, and neutrophil infiltration (myeloperoxidase assay)
were determined. The effect of TNF- on neutrophil infiltration was
assessed by neutralizing TNF- with TNF binding protein (TNF-BP)
before left renal I/R injury. TNF- protein expression, TNF- mRNA
induction, and neutrophil infiltration increased significantly in both
kidneys after unilateral renal I/R injury. Furthermore, the
administration of TNF-BP before unilateral renal I/R substantially
reduced the degree of neutrophil infiltration bilaterally. These
results constitute the initial demonstration that unilateral renal I/R
induces bilateral TNF- production and neutrophil infiltration
through a TNF--dependent mechanism.
tumor necrosis factor binding protein; myeloperoxidase; neutrophil; cytokine; inflammation
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