Acute tubular injury (acute tubular necrosis)
- Lesion
Tubular cells injured by poor blood flow or toxins slough off, block tubules and leak filtrate: the commonest cause of acute kidney injury in hospitals.
What it is
Acute tubular injury is damage to tubular epithelium that causes a rapid fall in GFR. Ischemia from shock, sepsis, surgery or bleeding hits the vulnerable straight segment of the proximal tubule and the thick ascending limb; toxins such as aminoglycosides, contrast media, cisplatin, ethylene glycol, heavy metals, myoglobin and hemoglobin hit mainly the proximal convoluted tubule. The injury is potentially reversible because tubular cells regenerate if the basement membrane survives. Deep jaundice can add bile cast nephropathy.
Structure
- Kidneys swollen with pale cortex and congested medulla.
- Proximal tubular cells lose their brush border, flatten, vacuolate or detach; lumens dilate.
- Casts of Tamm-Horsfall protein, cell debris and pigment in distal tubules and collecting ducts.
- Interstitial edema and leukocytes in the vasa recta; regenerating epithelium with mitoses in recovery.
- Bile cast nephropathy: green-brown bile casts in distal tubules with injured epithelium.
Step by step
- Ischemia or toxins injure tubular cells, which lose polarity and their brush border.
- Cells slough into the lumen and, with proteins, form casts that block urine flow.
- Pressure rises behind the obstruction, and filtrate leaks back through the damaged epithelium.
- More sodium reaches the macula densa, and tubuloglomerular feedback constricts afferent arterioles.
- Injured endothelium and inflammatory cells worsen medullary blood flow.
- If the basement membrane remains, surviving cells proliferate and restore the tubule within weeks.
Types of acute tubular injury
| Type | Causes | Pathology |
|---|---|---|
| Ischemic | Shock, sepsis, hemorrhage, major surgery | Patchy, short segments, basement membrane breaks |
| Pigment | Rhabdomyolysis (myoglobin), intravascular hemolysis (hemoglobin) | Red-brown pigmented casts |
| Nephrotoxic drugs and poisons | Aminoglycosides, contrast, cisplatin, ethylene glycol, mercury | Diffuse proximal necrosis; oxalate crystals with ethylene glycol |
| Bile cast | Severe hyperbilirubinemia, liver failure | Bile-stained casts in distal tubules |
Clinical notes
- Oliguria after hypotension, crush injury, sepsis or contrast exposure; potassium and acid accumulate.
- The recovery phase brings large volumes of urine and can cause hypokalemia and dehydration.
- Snake envenomation and leptospirosis, important in Colombia, can cause pigment or ischemic tubular injury.
In the lab
- High fractional excretion of sodium and urine that cannot be concentrated separate tubular injury from prerenal azotemia.
Test yourself
Think of the answer, then tap the question to see it.
Which urine casts suggest acute tubular injury?
Muddy brown granular casts with renal tubular epithelial cells.
Which tubular segments are most vulnerable to ischemia?
The straight portion of the proximal tubule and the thick ascending limb in the outer medulla.
Why can acute tubular injury recover?
Tubular epithelium regenerates when its basement membrane remains intact.
What is the danger of the polyuric recovery phase?
Large losses of water, sodium and potassium, causing hypokalemia and dehydration.
Elsewhere in DurgiPedia
- Patterns of necrosis: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous
- Shock: types, stages and the organs it damages
- Hypoxia, ischemia and reperfusion injury
- Physiology of acute and chronic kidney failure
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Acute tubular necrosis: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Acute Kidney Injury (StatPearls (NCBI Bookshelf), 2024).
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Representative model, for educational purposes only.