This study reports the pattern of renal injury in 24 North American children with hemolytic uremic syndrome (HUS), and the extent of extrarenal involvement in 9 of these children examined at autopsy. Fifteen of the 24 children were studied during the first 16 days of hospitalization; their renal specimens demonstrated glomerular thrombotic microangiopathy (TMA) in 8 children, cortical necrosis in 1, and varying degrees of glomerular TMA and cortical necrosis in 6 children. Nine of the children were studied after 16 or more days of hospitalization; these patients had prominent renal arterial lesions. Of 9 children examined at autopsy, extrarenal microthrombi were identified in 8. In 4 children who died during the acute phase of the disease, hemorrhagic colonic necrosis (3 children) and pancreatic islet cell necrosis (2 children) were the principal extrarenal lesions encountered. Rare microthrombi were present in the brains of the 3 children who manifested seizures.
Summary. Expression of the hapten fucosyl-N-acetyltactosamine was correlated with ultrastructural development in human granulocyie precursors using the monoclonal antibody FMC 10 with immunogoid techniques. The antigen was detectable from ihe myeloblast/early neutrophilic promyelocyte stage onwards and was associated with striking development of ihe rough endoplasmic reticular system. In addition, low levels of labelling were seen on monocytes, eosinophils and some basophll precursors. Coniraciion and alignment of the cisternae of the rough endoplastnic reiiciilum during the promyelocyte stage of neutrophilic differentiation gave the appearance of a plasma cell. However, on closer examination it was apparent that irue plasma cells did not react with this aniibody.
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