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'Acute tubular necrosis' or ('ATN') is a medical condition involving the death of tubular cells that form the 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 renal failure to the point that the two concepts are used interchangeably. 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 they are highly sensitive to due to their very high metabolism.

Contents

Toxic ATN

Ischemic ATN

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Toxic ATN

Toxic ATN can be caused by free hemoglobin or myoglobin, by medication such as antibiotics and cytostatic drugs, 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, obliterating it, and determining acute renal failure. Basement membrane is intact, so the tubular epithelium regeneration is possible. Glomeruli are not affected.

Ischemic ATN

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.

External links

★ Photo at: Atlas of Pathology

★ Acute Tubular Necrosis