We established a swine model of traumatic hemorrhagic shock to assess secondary renal injury under dry-heat conditions to clarify the roles of cell pyroptosis and inflammatory response in traumatic hemorrhagic shock development. Sixty-eight domestic Landrace piglets were divided into normothermic environment, dry-heat sham surgery, and dry-heat environment traumatic hemorrhagic shock groups (four subgroups: 3 h of environmental exposure and 60, 120, and 180 min after inducing traumatic hemorrhagic shock). The kidneys and blood were sampled at various time points. Univariate analysis of variance or non-parametric test was used for intergroup and intragroup comparisons, and the least significant difference test was used for multiple comparisons. The serum lipopolysaccharide, neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, blood urea nitrogen, and creatinine levels, as well as various inflammatory factors, oxidative stress indicators, and Paller score, were significantly higher under dry-heat environment traumatic hemorrhagic shock than under normothermic environment and dry-heat sham surgery at 180 min. The histopathological damage in the dry-heat environment traumatic hemorrhagic shock group increased significantly at 180 min. Immunohistochemistry, western blotting, and terminal deoxynucleotidyl transferase dUTP nick end labeling assays showed that protein expression and apoptosis index values in the renal tissues of all three groups increased but were significantly higher under dry-heat environment traumatic hemorrhagic shock than under normothermic environment and dry-heat sham surgery at 180 min. The combination of dry-heat environment and traumatic hemorrhagic shock induces an aggravation of secondary renal injury, which may be related to cell pyroptosis, inflammatory response, apoptosis, and oxidative stress. Our findings may assist in the development of treatments for acute kidney injury.