Our in silico studies supported such observations, as genes responsible for CRP and D-dimer elevation were found to be common in AKI-associated pathways, particularly IL-6/JAK-STAT, NF-κB, HIF-1, and complement pathways, ultimately causing renal microthrombosis, tubular necrosis, and fibrotic remodeling. This evidence concerns the gene NFKB1 and acute kidney injury.