Acute vs Chronic Tubular Injury

Exam map for tubular necrosis/injury: causes → pathogenesis → morphology → labs → clinical course. Tap tabs to switch the view.

1. Triggers

Ischemia: shock/sepsis/burnsNephrotoxinsAminoglycosidesAmphotericin BCisplatinRadiocontrastMyoglobin / hemoglobin

↓ renal perfusion or direct tubular toxin

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ATP depletion + mitochondrial injury

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Loss of brush border + tubular epithelial cell necrosis/apoptosis

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Tubular obstruction + back-leak of filtrate

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↓ GFR → acute kidney injury

Ischemic ATN: patchy necrosis along tubule, tubular rupture, interstitial edema; straight proximal tubule and thick ascending limb vulnerable.

Toxic ATN: more prominent proximal tubular epithelial necrosis, often segmental.

Muddy brown granular castsFeNa > 2%Urine Na⁺ > 40 mEq/LUrine osmolality < 350 mOsm/kgBUN:Cr ~ 10–15:1

Trap: FeNa may be low in contrast nephropathy, rhabdomyolysis, early sepsis, or diuretic use.

Initiation: hours–days after insult

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Maintenance: oliguria, azotemia, hyperkalemia, metabolic acidosis

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Recovery: polyuric phase as tubules regenerate; risk of hypokalemia/dehydration