The current study showed that SAR131675 treatment lowered systemic dyslipidemia and the levels of inflammatory cytokines, and ameliorated lipotoxicity-induced inflammation—as reflected by reduced MCP-1 and TNF-α expression and M1 macrophage infiltration and oxidative stress in the kidneys, thus suppressing glomerulosclerosis, tubulointerstitial fibrosis, and apoptotic renal cell death. The gene discussed is CCL2; the disease is glomerulosclerosis.