Involvement of Innate Immune System in the Pathogenesis of Sepsis-Associated Acute Kidney Injury

Although experimental models have shown that the innate immune system is a main contributor to acute kidney injury (AKI), its involvement in human sepsis-associated AKI (SA-AKI) remains unclear. We retrospectively evaluated 19 patients with SA-AKI who were treated with continuous renal replacement therapy (CRRT). Serum cytokine, complement components, and the proportion and functions of innate immune cells, such as CD56(+) T cells, CD56(+) natural killer (NK) cells, and monocytes, were analyzed. There were no differences in the proportions of CD56(+) T and NK cells between patients with SA-AKI and healthy controls. In patients with SA-AKI, fas ligand (FasL) expression in CD56(+) T cells was significantly upregulated, and the proportion of perforin-positive CD56(+) T cells tended to be higher than that in healthy controls. The positive rate of both FasL and perforin of CD56(+) T cells was significantly higher than that of CD56(-) T cells, which include cytotoxic T cells. Antigen-presenting capacity and phagocytic activity of monocytes in patients with SA-AKI were significantly decreased compared to those of healthy controls and did not recover soon after the initiation of CRRT. CD56(+) T cells are involved in the disease processes of human SA-AKI through effector molecules such as FasL or perforin.