LCN2 and acute kidney injury: However, most NGALs are monomeric (with a molecular weight of 25 kDa) and are mainly produced by injured kidney tubule epithelium.[26] NGAL levels increase rapidly during a proximal tubular injury and, thus, have emerged as a promising predictor of AKI.[27] Further, NGAL represents a critical component of bacterial infectious crisis.[6] Based on these reasons, NGAL is related to systemic inflammations rather than brain injury.