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Articles in PresS, published online ahead of print September 20, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00160.2001
Submitted on May 25, 2001
Accepted on September 5, 2001
1 Nephrology, The University of Chicago, Chicago, IL, USA
2 Pathology, Johns Hopkins University, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: rquigg{at}medicine.uchicago.edu.
Ischemia reperfusion injury (IRI) is a complex and incompletely understood process involving a cascade of events culminating in apoptotic and/or necrotic cell death. Natural IgM antibodies and complement have been implicated in the pathogenesis of IRI in a variety of organ systems, as have T lymphocytes in renal IRI. To investigate the role of immunoglobulins and T lymphocytes in renal IRI, recombination activating gene (RAG) 1 deficient mice were studied. RAG1 -/- mice were not protected from acute renal failure induced by 27.5 min of bilateral renal ischemia followed by reperfusion (serum urea nitrogen levels 30 h after reperfusion of 155.2 ± 5.6 and 152.8 ± 11.4 mg/dl in RAG1 -/- and wild-type mice, respectively, n = 13 each). Histological examination showed acute tubular necrosis and neutrophilic infiltration, with no significant differences between groups. In contrast to other organ systems, immunoglobulins were not found in kidneys at time points ranging from 1 min to 30 h following ischemia. Thus, immunoglobulins and mature T lymphocytes do not appear to play a significant role in the pathogenesis of IRI in the kidney.
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