Objective To construct and identify macrophage-conditional Atg 5-knockout mice to provide an animal model for studying the role of macrophage autophagy in the pathogenesis of renal diseases. Methods LysM-Cre mice were hybridized with Atg 5^{flox/ +} mice, and Atg 5^{flox/ +} mice were self-crossbred to obtain progeny mice with Atg 5^{flox/ +} Cre ^{+/ -} and Atg 5flox/ flox Cre ^{-/ -} . The progeny mice of the above two genotypes were then hybridized to obtain macrophage-conditional Atg 5 gene-knockout mice ( Atg 5flox/ flox Cre ^{+/ -} , Atg 5 ^{-/ -} ) and control mice ( Atg 5flox/ flox Cre ^{-/ -} , Atg 5+/ + ). The phenotypes of the mice were determined via electrophoresis of DNA that had been extracted from mouse tail tissue and amplified via PCR. Mouse bone marrow-derived macrophage RNA and protein were extracted, and Atg 5 gene expression was tested via sequencing and Western blotting. Results A macrophage-conditional Atg 5-knockout mouse model was established; these mice survived and were fertile. The macrophage Atg 5 gene was successfully knocked out at both the gene and protein levels. The basic macrophage autophagy level in the Atg 5 ^{-/ -} mice was much lower than that in the Atg 5+/ + mice (p62 was significantly increased, and LC3II was significantly reduced) and could not be restored to the basic level without deleting Atg 5 after stimulation with the autophagy activator rapamycin. Conclusions Macrophage-conditional Atg 5 - knockout mice are successfully constructed and identified via the Cre / loxp system, providing a research platform for studying the role of macrophage autophagy in renal disease pathogenesis at the animal level.