We studied renal venous blood after renal infection for its concentrations of leukocytes, complement and renin. In addition, we evaluated this blood for granulocytic aggregation and chemiluminescence of granulocytes. We found that very rapid activation of serum complement occurred with associated granulocytic aggregation and evident vascular occlusion and ischemia since renin rose rapidly. It appears that this early sequence of events will cause renal damage by ischemic change, as well as that known to occur from the inflammatory reaction.
Rhesus monkeys (Macaca mulatta) were immunized with purified P fimbriae from Escherichia coli during the last trimester of pregnancy. Infants born of these mothers were compared with those from nonimmunized rhesus mothers. A delay in the onset of renal disease after bladder infection showed protection from passive immunization. This was associated with a high antibody titer in serum. In addition to delayed onset of renal infection, a decreased number of immunized monkeys developed pyelonephritis.
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