To detect CS-AKI at an early stage, traditional biomarkers such as sCr levels and urine output have important limitations. Stress markers, such as tissue inhibitor of metalloproteinases-2 and insulin-like growth factor binding protein 7, as well as damage markers like the neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, and liver fatty acid-binding protein, have enabled a more precise delineation of the etiology, pathophysiology, site, mechanisms, and severity of injury, enabling early diagnosis and prognostication of AKI [25]. This evidence concerns the gene FABP1 and Cowden syndrome 1.