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Pathological Anatomy · Diseases of the Kidneys and Urinary Tract

Acute tubular necrosis

Necrosis tubulorum acuta

Acute tubular necrosis (Necrosis tubulorum acuta) is a reversible renal injury caused by impaired blood flow due to shock or severe hypotension. This pathology is characterized by destruction of the tubular epithelium and is the leading cause of acute kidney injury.

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Main cause of AKIThe most frequent etiology of acute kidney injury
Criterion for AKIOliganuria: urine output less than 400 ml per day
ClassificationIschemic, pigmentary, and nephrotoxic types
Stages of AKIShock, oliguric, and diuresis recovery stages
2 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Causes and classification

There are three main varieties of acute tubular necrosis (Necrosis tubulorum acuta), each with its own triggering factors:

  • Ischemic ATN: develops during systemic shock and a sharp drop in blood pressure.
  • Pigmentary ATN: clinically and morphologically similar to ischemic ATN. It occurs due to hemolysis with hemoglobinuria (during incompatible blood transfusions or crises) or rhabdomyolysis with myoglobinuria in severe muscle trauma.
  • Nephrotoxic ATN: essentially a variant of ischemic injury triggered by drugs (e.g., antibiotics like gentamicin), radiocontrast agents, poisons (mercury), or organic solvents.

Pathogenesis and mechanisms of oliguria

The central link of the pathology is damage to the tubular epithelium, which is highly sensitive to anoxia and toxins. The renal medulla suffers first due to the specific features of its blood supply.

The development of oliguria and renal failure is driven by a complex of mechanisms:

  1. Tubuloglomerular feedback: tubular damage causes constriction of the afferent arterioles, which reduces filtration in the glomeruli.
  2. RAAS: activation of the renin-angiotensin system increases vascular spasm.
  3. Tubular obstruction: cellular breakdown products (detritus) and protein casts block urine flow, increasing intratubular pressure.
  4. Backleak (backleak): seepage of fluid from destroyed tubules into the interstitium leads to compression of nephrons.
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Morphological picture

In ischemic acute tubular necrosis, focal necrosis, basement membrane ruptures (tubulorrhexis), and lumen occlusion by casts are observed. The straight segments of the proximal tubules and the thick ascending limb of the loop of Henle in the medulla are the most vulnerable.

In the distal segments and collecting ducts, casts are formed from Tamm-Horsfall protein mixed with hemoglobin and myoglobin. The interstitium becomes edematous, and leukocytes accumulate in the dilated vessels (vasa recta). Later, regeneration begins: cells flatten, mitotic figures appear, which can lead to complete restoration of the structure.

Toxic ATN predominantly affects the proximal convoluted tubules. Each agent leaves distinct changes:

  • Corrosive sublimate (mercury chloride) produces large acidophilic inclusions and calcification.
  • Carbon tetrachloride causes lipid infiltration.
  • Ethylene glycol leads to vacuolar degeneration and the appearance of calcium oxalate crystals.

Class and exam questions

What serves as the main morphological sign of ischemic ATN?

Focal necrosis with basement membrane damage (tubulorrhexis), protein cast formation in the distal segments, and pronounced interstitial edema.

What blood supply features make the renal medulla vulnerable?

The medulla receives a smaller fraction of the total renal blood flow, which is why it reacts more acutely to ischemia and hypotension.

What are the casts found in the tubules in ATN made of?

They consist of Tamm-Horsfall protein mixed with plasma proteins, as well as myoglobin or hemoglobin.

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What else to study on this topic

  • The etiological role of intrarenal vessel obstruction and glomerulonephritis in the development of AKI
  • Detailed analysis of the stages of acute kidney injury
  • Mechanisms of action of toxic agents: mercury salts and ethylene glycol
  • The role of Tamm-Horsfall protein in health and disease
  • Cellular processes of tubular epithelial regeneration

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