Paper Information

Title: 

ISCHEMIC AND NON-ISCHEMIC ACUTE KIDNEY INJURY CAUSE HEPATIC DAMAG

Type: POSTER
Author(s): GOLAB F.*,KADKHODAEI MEHRI,ZAHMATKESH MARYAM,HEDAYATI S.M.,ARAB H.,SOLEYMANI MANOUCHEHR
 
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Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

Recent studies have documented that remote organs are affected by ischemic injury to the kidney. Here we studied whether the liver also suffers damage during induction of renal ischemia reperfusionin rats and compared this to bilateral nephrectomy. Hepatic levels of tumor necrosis factor-alphaincreased significantly after 6 and 24 h of renal ischemia or nephrectomy. Malondialdehyde, an index of lipid peroxidation, increased while total glutathione was decreased in the liver in both the renal ischemia and nephrectomy groups, suggesting activation of oxidative stress. Expression of liver spermine-spermidine acetyl transferase, an enzyme upregulated in early phases of hepatic injury was significantly increased 6 h after either kidney ischemia or nephrectomy. Apoptosis was increased in hepatocytes 24 h after nephrectomy. We also found histological evidence of hepatocyte injury following both ischemia and bilateral nephrectomy. Infusion of reduced glutathione, before the induction of renal ischemia, significantly improved liver architecture and was associated with areduction in hepatic malondialdehyde and serum alanine transaminase levels. Our study shows that acute kidney ischemia or renal failure activates oxidative stress and promotes inflammation, apoptosis, and tissue damage in hepatocytes.

 
Keyword(s): REMOTE ORGANS, ISCHEMIA REPERFUSION, BILATERAL NEPHRECTOMY.A
 
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