investigate the role of Fabp4 on urolithiasis. 2)An in vitro study using murine renal tubular cells (RTC) was conducted to examine calcium oxalate crystallization via Fabp4. We compared the control group with the Fabp4 knockdown group after 6 hours exposure of calcium oxalate monohydrate (COM).RESULTS: 1)The Fabp4 KO mice had significantly larger amounts of renal crystal deposits and urinary crystal than the WT mice. Additionally, the gene expression level of Ccl2 was lower in the Fabp4 KO mice than in the WT mice (figure 1A). The RNA-sequence result demonstrated that there were 16 genes commonly differentiated (>2fold) before and after renal crystal development in the Fabp4 KO mice compared with the WT mice. These genes were associated with downregulation of antioxidant activity, IgA binding, and Toll-like receptor binding; cell-cell adhesion and neutrophil aggregation; and IgA immunoglobulin complex in Gene Ontology analysis.2)In the Fabp4 knockdown RTC, COM crystal endocytosis rate was significantly lower than the control. Gene expression levels of Ccl2 and Tumor necrosis factor were higher in the Fabp4 knockdown RTC than those of the control (figure 1B).CONCLUSIONS: We have found that Fabp4 deficiency suppresses macrophage function and crystal endocytosis in renal tubular stones, leading to stone development. These data support a causal role for FABP4 in driving urinary stone formation.

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