There are different AKI biomarker types: an increased urinary excretion of proximal tubule proteins due to tubular damage (e.g., N-acetyl-β-d-glucosaminidase), proximal tubular dysfunction detected by decreased tubular reabsorption of filtered proteins (e.g., cystatin C), tubular genes and proteins immediately upregulated in response to injury (e.g., kidney injury molecule-1 KIM-1, neutrophil gelatinase-associated lipocalin), and urinary excretion of injury-induced mRNA levels (e.g., vanin-1, monocyte chemotactic peptide-1 (MCP-1)) [2,3,4,5,6]. This evidence concerns the gene CST3 and acute kidney injury.