Background and purpose:
Hyperuricemia is an essential risk factor in chronic kidney disease
(CKD), while urate-lowering therapy to prevent or delay CKD progression
is controversial. Alternatively activated macrophages in response to
local microenvironment play diverse roles in kidney injury, repair, and
fibrosis. Here, we aim to investigate whether and how macrophage ITGAM
contributes to hyperuricemia-related CKD.