Pathology of the urinary system

Nephrotoxic tubular necrosis (exogenous toxic nephrosis)

 

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caused by ingestion of a wide variety of exogenous substances such as oxalates, heavy metals, plant 

toxins, antibiotics, etc.; the kidney is the primary target organ for many toxicoses; 

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the basement membranes are preserved, thus the potential for repair is good if the animal survives 

the acute phase; 

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kidneys are pale and swollen, and the parenchyma bulges when the capsule is cut; 

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microscopically, the tubular necrosis is extensive; 

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some substances like oxalates precipitate as crystals in the tubules (best seen with polarized light); 

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accidental ingestion of antifreeze (ethylene glycol) is a frequent cause of severe acidosis and renal 

failure in cats and dogs; in pig barns, ethylene glycol poisoning can occur when antifreeze solution is 

added to the water lines as the barn sits empty between groups of animals and the lines are not 

flushed properly prior to the arrival of a new group; 

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ethylene glycol (via hepatic alcohol dehydrogenase) → glycoaldehyde → glycolic acid (the 

primary toxic metabolite, which can cause fatal acidosis) → glyoxylic acid → oxalic acid → 

calcium oxalate (soluble complex) → filtered by glomerulus → precipitates as crystals in 

lumina of renal tubules (as water is reabsorbed and pH drops); 

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most metabolic by-products of ethylene glycol are filtered through the glomerulus, and all 

may have a direct toxic effect on the renal tubular epithelium, causing degeneration and 

necrosis. 

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large doses of ascorbic acid (vitamin C) have caused oxalate nephrotoxicosis in humans; ascorbic 

acid is a metabolic precursor of oxalate.