Kidney hyperfusion induces immunological reactions in glomeruli (LB525)

Objectives. Endothelium is the first line of contact with immune system. It is known that activated lymphocytes impair endothelial functions. However, whether endothelial dysfunction could initiate immune reaction remains unclear. Methods. C57/BL6 mice were randomly grouped into sham‐operated (2K), 1 kidney removal (1K) and 5/6 nephroectomy groups (5/6K‐off). Mouse glomeruli were collected for polymerase chain reaction (PCR) and immunohistochemistry study. Results. Four weeks after nephrectomy 5/6K‐off mice had a significantly higher level of renal blood flow, compared with 2K and 1K groups. Urine protein levels, which were normalized with remaining glomeruli, were similar in the three groups. There were no significant increase in levels of macromolecules in urine samples of 5/6K‐off group. Glomerular filtration experiments also supported it. These results suggested that glomeruli of 5/6K‐off group have normal function. In PCR experiments, the expressions of major histocompatibility complex Q lotus, but not the major histocompatibility complex T lotus, were significantly increased in both 1K and 5/6K‐off groups. mRNA expression of both CD80 (B7‐1) and CD86 (B7‐2), costimulatory signals for T cells, were significantly increased in 1K and 5/6K‐off groups. These finding suggests that kidney hyperfusion could initiate immune reaction. Complement component 5a receptor mRNA expression was increased, whereas complement decay‐accelerating factor (also known as CD55) expression was decreased in 5/6K‐off group. Conclusion. The present study suggests that kidney hyperfusion induces immunological reactions in glomeruli. The complement pathway plays important roles in these reactions. Further experiments will focus to identify the underlying mechanisms. Grant Funding Source : National Natural Science Foundation of China 81373412