We identified AKI-relevant modules that were activated in chemical exposure conditions causing kidney injury and which contained well-known AKI-relevant genes such as Havcr1, Clu, and Tff3. We used the genes in these modules to 1) generate a signature for predicting kidney injury that performed better than well-known AKI biomarkers, and 2) identify pathways and networks of extracellular matrix (ECM)-receptor interactions, glutathione metabolism, and p53 signaling pathways associated with kidney injury. Here, HAVCR1 is linked to acute kidney injury.