*Purpose: Ischemia reperfusion injury (IRI) perpetuates inflammation and causes significant organ injury in solid organ transplantation. CD38 is a ectoenzyme widely expressed on lymphocytes with important functions in NAD metabolism, calcium modulation, and cellular adhesion to vascular endothelium. Pharmacologic inhibition and genetic deletion of CD38 preserve vasodilatory and contractile function and protect against myocardial infarction in ex vivo models of cardiac IRI. The purpose of this study is to investigate the role of CD38 in renal IRI.

*Methods: Male wild-type and CD38 KO C57BL/6 mice were subjected to forty minutes of unilateral warm renal IRI by exposing the left renal pedicle and clamping the renal artery and vein. During the ischemic interval temperature was rigorously maintained at 35-37 degrees Celsius. Twenty-four hours after the ischemic insult the left (post-ischemic) and right (control) kidneys were removed and flushed. Following collagenase digestion flow cytometry was used to quantify lymphocytic infiltration into the kidneys.

*Results: CD38 KO mice had significantly reduced numbers of neutrophils per gram of renal parenchymal tissue compared to wild-type controls (1.7 x 10⁶ cells/gram tissue vs. 3.99 x 10⁶ cells/gram tissue, P = 0.047, Figure 1). There were no significant differences found in the T cell, monocyte or macrophage lineages.

*Conclusions: Congenital absence of CD38 results in reduced infiltration of neutrophils into post-ischemic kidneys and protection from renal ischemia reperfusion injury.

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