Human AKI is manifested by inflammation, and an early feature in the pathogenesis is the
accumulation of immune cells in the kidney. To understand the pathophysiology of AKI,
results from animal models have shown a causal relation between the leukocyte activation
and infiltration to the kidney after kidney ischemia-reperfusion. Blocking the activation or
trafficking of proinflammatory leukocytes into the kidney preserves renal function and
histologic integrity. In contrast, the anti-inflammatory lymphocytes called regulatory T cells …