Acute tubular necrosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Pathophysiology
Toxic Acute Tubular Necrosis
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").
Ischemic Acute Tubular Necrosis
Ischemic Acute Tubular Necrosis 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 Acute Tubular Necrosis specifically causes skip lesions through the tubules.
Microscopic Pathology
Acute tubular necrosis from ethylene glycol
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.
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