Genetic susceptibility to renal ischemia reperfusion injury revealed in a murine model

Transplantation. 2000 Mar 15;69(5):1023-5. doi: 10.1097/00007890-200003150-00065.


Background: The development of genetically engineered mice has led to increased use of mouse models to study renal ischemic reperfusion injury (IRI). We hypothesized that susceptibility to IRI could result from strain differences due to genetic factors.

Methods: Our study compared recovery subsequent to renal IRI in NIH Swiss, C57BL/6, and BALB/c mice. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were evaluated postischemia. We also conducted reverse transcriptase-polymerase chain reaction (RT-PCR) analyses of renal cytokines and adhesion molecules postischemia.

Results: At 48 hr postischemia, renal dysfunction in NIH Swiss mice was significantly reduced, compared with other groups (P<0.01). BUN measurements confirmed renal protection at 48 hr in the NIH Swiss group. RT-PCR analysis of mRNA postischemia demonstrated that, between strains, there was little difference in mRNA expression for renal cytokines and adhesion molecules.

Conclusions: NIH Swiss mice appear to be resistant in susceptibility to renal IRI. Early expression of pro-inflammatory genes was not associated with resistance to IRI, thus genetic factors could be important in outcome after renal IRI.

MeSH terms

  • Animals
  • Blood Urea Nitrogen
  • Cell Adhesion Molecules / genetics
  • Creatinine / blood
  • Cytokines / genetics
  • Genetic Predisposition to Disease*
  • Ischemia / genetics*
  • Kidney / metabolism
  • Kidney / physiopathology
  • Mice / genetics
  • Mice, Inbred BALB C / genetics
  • Mice, Inbred C57BL / genetics
  • Postoperative Period
  • RNA, Messenger / metabolism
  • Renal Circulation*
  • Reperfusion Injury / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction


  • Cell Adhesion Molecules
  • Cytokines
  • RNA, Messenger
  • Creatinine