In nephrocalcinosis-related CKD mice, deposition of oxalate crystal and tubular injury are associated with activation of NLRP3 inflammasomes; inhibition of NLRP3 induces a shift of macrophages from CD45+F4/80+CD11b+CX3CR1+CD206−, an M1 pro-inflammatory state, to CD45+F4/80+CD11b+CD206+TGFβ−, an M2 anti-inflammatory phenotype, and attenuates the progression of CKD [48]. This evidence concerns the gene NLRP3 and nephrocalcinosis.