FUNCTION RECOVERY PATTERN IN ACUTE RENAL FAILURE FOLLOWING INGESTION OF MERCURIC CHLORIDE

THE CHARACTERISTIC renal lesion produced by mercuric chloride has been described as being confined largely to the proximal tubule.¹ Large doses of mercury tend to produce necrosis extending the whole length of the proximal tubule from the glomerulus to the descending loop, while smaller doses appear to affect selectively the more distal portions of the proximal convolution and its medullary portion.² Subnecrotizing doses may produce no more than swelling of the epithelium, presumably, in the more distal segments of the proximal nephron.

Recently Oliver and associates³ have drawn attention to a second type of tubular lesion which may be found in cases of poisoning with corrosive mercuric chloride and which is indistinguishable from that found in shock-like states such as following crushing injuries and transfusion of incompatible blood. The second type of lesion differs from the nephrotoxic lesion found uniformly in the proximal nephron; it consists of