In our editorial in the Journal in 1978,1 Kaplan and I discussed the observations of Koster et al.2 on shigella-associated hemolytic uremic syndrome, which suggested that endotoxin damaged vascular endothelium and set in motion events leading to the full-blown syndrome. We were concerned that others had not observed endotoxemia in this syndrome and that this pathogenetic mechanism might apply in a limited number of cases.We emphasized that in parallel with the nephrotic syndrome, the hemolytic uremic syndrome could be seen as a constellation of clinical and laboratory findings occurring in many different settings and resulting from a variety of . . .
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Keith N. Drummond (1985) studied this question.
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