Interleukin-18 binding protein attenuates renal injury of adriamycin-induced mouse nephropathy.

Nephrotic syndrome is one of the most common kidney diseases in children, most of which were caused by minimal change disease, which could be typically reversible with the use of corticosteroid therapy in steroid-sensitive nephrotic syndrome. At the same time, there still exist some side effects caused by drugs and steroid-resistant nephrotic syndrome. It's urgent to investigate more accurate treatment to improve the situation. In this study, we chose mice model by adriamycin to observe the effect of IL-18BP intervention. It was shown that (1) weak general conditions appeared after adriamycin administration; (2) Proteinuria showed up after adriamycin-administration and then decreased with IL-18 binding protein intervention; (3) the level of triglyceride, cholesterol, IL-18, IFN-γ, and TNF-α in the IL-18 binding protein intervening group were significantly lower than those in the adriamycin-minimal change disease MCD group (all P < 0.01), and the levels of serum total protein, albumin, and IL-4 were significantly higher than those in the adriamycin-minimal change disease MCD group (P < 0.05, P < 0.01, P < 0.05); (4) ultramicrostructural examination demonstrated wide fusion of foot processes of glomerular epithelial cells in adriamycin-minimal change disease MCD mice, while only focal fusion occurred in IL-18 binding protein intervening mice. In conclusion, IL-18BP repaired the proteinurine, histopathological injury of kidney, and the induction of serum cytokines in mice models of minimal change disease induced by adriamycin. IJCEP