The most common cause of acute kidney injury (AKI) is ischemia, which refers to reduced blood flow to the kidneys. Measures to correct underlying causes of acute kidney injury (AKI) should begin at the earliest indication of kidney dysfunction. Serum creatinine does not rise to abnormal levels until a large proportion of the renal mass is damaged, because the relationship between the glomerular filtration rate (GFR) and the serum creatinine level is not linear, especially early in the disease. Indeed, the rise of serum creatinine may not be evident before 50% of the GFR is lost. It cannot be overstated that the current treatment for AKI is mainly supportive; no therapeutic modalities to date have shown efficacy in treating the condition. Therapeutic agents (eg, dopamine, nesiritide, fenoldopam, mannitol) are not indicated in the management of AKI and may be harmful to the patient. Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary