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.