Peritubular capillaries. A major target site of endotoxin-induced vascular injury in the primate kidney.

We have examined by light and electron microscopy the kidneys of rhesus monkeys infused either with a single bolus of endotoxin (10 mg. per kg.) or continuously at the rate of 10 mg. per kg. per hour for periods of up to 22 hours. Controls included monkeys infused with Ringer's lactate solution. Only minor morphologic changes were seen in animals receiving a bolus of endotoxin. In the animals continuously infused, sequestration of neutrophils and monocytes was observed in the peritubular capillaries and to a lesser extent in the glomeruli. These changes were associated with phagocytosis of endotoxin, occasional fibrin deposits, and extensive endothelial cell damage with focal capillary disruption. Changes found in the advanced stages included prominent interestitial edema with focal necrosis of tubular epithelium. Endothelial cell changes seen in the glomeruli were far less sever than those observed in the peritubular capillaries. Our data indicate that endothelial damage and associated events relating to the sequestration of phagocytic leukocytes primarily involve the peritubular capillaries and that this "inflammatory" process plays a basic role in the development of acute tubular necrosis during shock associated with endotoxemia.