Acute Tubular Necrosis

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Acute tubular necrosis

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 and is one of the most common causes of ARF.[1] The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN.[2]

Classification

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.[3]

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.[4]

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.

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