Pathology of the urinary system

Ischemic tubular necrosis (tubulorrhectic nephrosis)

 

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follows a period of hypotension (e.g. hypovolemic or neurogenic shock) or severe acute anemia (e.g. 

hemolytic crisis) which causes marked tubular ischemia; 

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can be associated with endogenous compounds which may exacerbate the tubular necrosis, e.g. 

 

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hemoglobin (hemoglobinuric nephrosis) in acute intravascular hemolysis (which causes 

anemia); 

 

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myoglobin (myoglobinuric nephrosis) in severe rhabdomyolysis (which causes hypotension); 

 

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neither hemoglobin nor myoglobin is a primary nephrotoxin, but intratubular casts formed by 

these molecules may exert deleterious pressure on the tubular epithelium; 

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the difference between acute tubular necrosis and renal cortical necrosis (see Circulatory 

Disturbances) is simply a question of degree of ischemia; in renal cortical necrosis, the whole cortex 

may be involved, and both glomeruli and tubules are destroyed; in acute tubular necrosis, the 

necrosis is more patchy and confined to segments of the proximal and distal convoluted tubules; 

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the damage involves tubular basement membranes, thus limiting the capacity for tubular epithelial 

repair; 

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gross lesions include swelling and, possibly, color change if accumulation of pigment is involved; 

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microscopically, the tubular necrosis is patchy; there are coagulation necrosis and exfoliation of the 

tubular epithelium and presence of hyaline casts (protein) in the tubular lumina. 

 

 

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