Acute Tubular Necrosis (ATN).

ischemic ATN:

hypovolemic shock due to severe trauma, acute pancreatitis, septicemia;
mismatched blood transfusions and other hemolytic crises, myoglobinuria in crush syndrome, which clogs the tubule causing ischemia

nephrotoxic ATN:

heavy metals (e.g., mercury); organic solvents (e.g., carbon tetrachloride); drugs such as gentamicin and other antibiotics, and radiographic contrast

3 stages

initiation phase, lasting about 36 hours

maintenance phase with marked anuria, uremia and fluid overload

Recovery phase: diuresis can casuse electrolyte imbalances.

straight portions of the proximal tubule and the ascending thick limbs are predominantly involved

attenuation of proximal tubular brush borders, blebbing and sloughing of brush borders, vacuolization of cells, and detachment of tubular cells into the lumen forming casts

Tamm-Horsfall protein

When crush injuries have produced ATN, the casts are composed of myoglobin

infiltrate consisting of polymorphonuclear leukocytes, lymphocytes, and plasma cells

If the patient survives for a week, epithelial regeneration becomes apparent in the form of a low cuboidal epithelial covering.

Possible pathogenetic mechanisms in ischemic acute renal failure.


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