Etiology of Acute Tubular Necrosis Common causes of acute tubular necrosis include the following: Renal hypoperfusion, most often caused by hypotension or sepsis (ischemic ATN; most common, especially in patients in an intensive care unit) Nephrotoxins Major surgery (often due to multiple factors) Other causes of ATN include Third-degree burns covering > 15% of body surface area The heme pigments myoglobin and hemoglobin (caused by either rhabdomyolysis or massive hemolysis) Other endogenous toxins, resulting from disorders such as tumor lysis or multiple myeloma Poisons, such as ethylene glycol Herbal and folk remedies, such as ingestion of fish gallbladder in Southeast Asia Common nephrotoxins include the following: Aminoglycosides Amphotericin B Cisplatin and other chemotherapy drugs Radiocontrast (particularly ionic high osmolar agents given IV in volumes > 100 mL—see Contrast Nephropathy) Nonsteroidal anti-inflammatory drugs (NSAIDs; especially when concurrent with poor renal perfusion or other nephrotoxic agents) Colistimethate (colistin) Calcineurin inhibitors (eg, cyclosporine, tacrolimus, used systemically) Vancomycin (particularly with supratherapeutic dosing [1]) Massive volume loss, particularly in patients with septic or hemorrhagic shock, pancreatitis, or major surgery, increases the risk of ischemic ATN; patients with serious comorbidities are at highest risk.