Twelve control dogs receiving a single intravenous injection of mercuric chloride, 3.0 mg. per kg., all died within 4 to 11 days afterwards with marked nitrogen retention and extensive necrosis and calcification of the epithelium lining the proximal convoluted tubules.
Three dogs of comparable age and weight were reduced to a standard hypoproteinemic state by repeated plasmapheresis. Each dog then received the same dose of mercuric chloride as the controls. None of these dogs became sick, none showed any elevation of non-protein nitrogen, and the kidneys— both in the gross and histologically—appeared normal when they were examined 8 to 45 days later.
As tested thus far intensive plasmapheresis following the injection of mercuric chloride has been without effect in preventing the classical changes of mercuric chloride injury observed in the control dogs.
The simplest explanation for these phenomena is that mercuric chloride acts on a more or less specific substance (presumably fabricated or concentrated in the renal cortex) which is depleted in the standard hypoproteinemic state. Other possibilities are mentioned.
These findings are in sharp contrast to the results of similar experiments with uranium nitrate. The hypoproteinemic state appears to render the animals more susceptible to uranium injury (3). This probably indicates that the mode of action of the two heavy metals is different.