Experimental studies on the hemolytic-uremic syndrome.
Ultrastructural studies of blood cells during the acute stage of the hemolytic-uremic syndrome (HUS) revealed striking, but transient, changes in erythrocyte structure. These included membrane disruption, vacuolar degeneration, and Heinz body formation. There was also evidence of platelet injury, and there were peculiar tactile interactions between histiocytes and impaired red cells. These changes disappeared as the patients recovered. These changes were considered to be important in the pathogenesis of the hemolytic and thrombolytic features of HUS, and studies were directed at reproducing them in vitro and in vivo. Treatment of red cells with purified clostridial phospholipase C induced changes in red cells and platelets that were comparable to those encountered in HUS. Rats infused with phospholipase C developed hemolysis, thrombocytopenia, and hemoglobinuria. Their kidneys did not, however, reveal glomerular alterations similar to those seen in patients with HUS. It is proposed that HUS in some cases might be initiated by a nonspecific infectious injury to the intestinal mucosa thereby allowing increased absorption of toxins derived from indigenous gut flora and that these toxins could be responsible for the hemolysis, thrombolysis, and even the renal injury.
D000818:Animals; D001792:Blood Platelets / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D004910:Erythrocyte Membrane / Q000648:ultrastructure; D004912:Erythrocytes / Q000187:drug effects / Q000473:pathology*; D005260:Female; D006366:Heinz Bodies / Q000648:ultrastructure; D006463:Hemolytic-Uremic Syndrome / Q000097:blood / Q000209:etiology / Q000473:pathology*; D006644:Histiocytes / Q000473:pathology; D006801:Humans; D007223:Infant; D007668:Kidney / Q000473:pathology*; D008297:Male; D008854:Microscopy, Electron; D051381:Rats; D010738:Type C Phospholipases / Q000494:pharmacology; D014617:Vacuoles / Q000648:ultrastructure
D010738:Type C Phospholipases