Acute Tubular Necrosis (ATN): Top Causes – Hypoperfusion and Nephrotoxins

Acute Tubular Necrosis (ATN) is the most common cause of intrinsic acute kidney injury (AKI). Two major etiologies dominate:

1. Ischemic ATN (Hypoperfusion) – ~50%

Renal hypoperfusion → tubular epithelial injury. Precipitants:

• Heart failure / cardiogenic shock
• Septic / hemorrhagic shock
• Severe dehydration / burns
• Major surgery (especially vascular, cardiac)
• Hepatorenal syndrome

2. Nephrotoxic ATN – ~35%

Direct tubular toxicity. Common agents:

• Aminoglycosides (gentamicin, amikacin) – proximal tubule accumulation.
• Vancomycin (trough >15–20 µg/mL).
• Contrast media (iodinated) – CIN/AKI.
• NSAIDs – afferent arteriolar constriction.
• Chemotherapy (cisplatin, ifosfamide).
• Heavy metals (lead, mercury, cadmium).
• Illicit drugs (cocaine, heroin, synthetic cannabinoids).
• Tumor lysis, rhabdomyolysis (intrarenal obstruction + toxicity).

Clinical Pearl

Muddy brown granular casts + fractional excretion of sodium (FeNa) >2% support ATN. Prevention: volume optimization, nephrotoxin avoidance/dose adjustment, NAC for contrast (controversial).