Further molecular experimental results indicate that the hyperuricemia mouse model exhibits a bidirectional imbalance in the uric acid transport system: in addition to the overexpression of URAT1 and GLUT9 on the brush border membrane of the proximal tubule, the mRNA and protein levels of basolateral ABCG2, OAT1 and OCT2 are significantly downregulated. Here, ABCG2 is linked to hyperuricemia.