Although many studies investigating urinary NGAL utility in predicting the development of AKI have normalized NGAL against creatinine to control changes in urine flow rate, the underlying assumption of constant creatinine excretion may be flawed.[38, 39] Lower creatinine excretion in the setting of acute GFR loss during early stage of AKI may amplify the NGAL performance irrespective of whether NGAL synthesis is increased by injury or not. The gene discussed is LCN2; the disease is acute kidney injury.