Acute tubular necrosis
|Acute tubular necrosis|
|Classification and external resources|
Acute tubular necrosis (ATN) is a medical condition involving the death of tubular cells that form the renal tubule that transports urine to the ureters while reabsorbing 99% of the water (and highly concentrating the salts and metabolic byproducts). Tubular cells continually replace themselves and if the cause of ATN is removed then recovery is likely. ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN.
It may be classified as either toxic or ischemic. Toxic ATN occurs when the tubular cells are exposed to a toxic substance (nephrotoxic ATN). Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition that they are highly sensitive and susceptible to, due to their very high metabolism.
Acute tubular necrosis is classified as a "renal" (i.e. not pre-renal or post-renal) cause of acute kidney injury. Diagnosis is made by a FENa (fractional excretion of sodium) > 3% and presence of muddy casts (a type of granular cast) in urinalysis. On histopathology, there is usually tubulorrhexis, that is, localized necrosis of the epithelial lining in renal tubules, with focal rupture or loss of basement membrane. Proximal tubule cells can shed with variable viability and not be purely "necrotic". 40_75%
Toxic ATN can be caused by free hemoglobin or myoglobin, by medication such as antibiotics such as aminoglycoside and cytoxic drugs such as cisplatin, or by intoxication (ethylene glycol, "anti-freeze").
Histopathology: Toxic ATN is characterized by proximal tubular epithelium necrosis (no nuclei, intense eosinophilic homogeneous cytoplasm, but preserved shape) due to a toxic substance (poisons, organic solvents, drugs, heavy metals). Necrotic cells fall into the tubule lumen, obturating it, and determining acute renal failure. Basement membrane is intact, so the tubular epithelium regeneration is possible. Glomeruli are not affected.
Ischemic ATN can be caused when the kidneys are not sufficiently perfused for a long period of time (i.e. renal artery stenosis) or during shock. Hypoperfusion can also be caused by embolism of the renal arteries. Ischemic ATN specifically causes skip lesions through the tubules.
- Photo at: Atlas of Pathology
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