Purpose of reviewThe pathophysiology of ischemic acute renal failure is complex, incompletely understood and there are no specific therapies. Descriptive observations in human acute renal failure, as well as mechanistic studies in animals, have demonstrated an important pathophysiological role for leukocytes and leukocyte adhesion molecules. The purpose of this review is to summarize and interpret the recent advances on the role of T cells and leukocyte adhesion molecules in ischemic acute renal failure.Recent findingsEmerging data suggest that the T cell is involved in modulating the outcome of ischemic acute renal failure, as well as ischemic injury to other organs. These new data build on the established role of inflammation in acute renal failure, and identify novel therapeutic targets. In addition, identification of the role of the T cell in the immediate injury response extends current immunological models of T cell function. Studies on leukocyte adhesion in acute renal failure have now identified the selectins and their ligands as important components of the inflammatory response to ischemic injury.SummaryThe identification of T cells and new adhesion molecule pathways as modulators of ischemic acute renal failure offers novel and feasible therapeutic opportunities for both native and transplant acute renal failure. Rigorous clinical trials are required to translate these basic findings to the bedside. In addition, mechanistic studies are needed to elucidate the molecular mechanisms by which these pathways modulate kidney injury. The identification of T cell engagement in ischemic renal injury can also help explain long-standing observations linking alloantigen-independent and alloantigen-dependent renal damage.