Ureteral blockade sensitizes to the generalized Shwartzman reaction.

Renal cortical necrosis (RCN) has been reported in the normal kidney of patients with a contralateral ureteral occlusion (UO). So far, studies have examined the mechanisms protecting the affected kidney from glomerular thrombosis and cortical necrosis; but to the authors' knowledge, none has ever investigated the potential role of UO on the occurrence of the associated disseminated intravascular coagulation (DIC) episode leading to RCN. Female rats with a ligature of the right or left ureter were given injections, at different times after surgery, of 400 micrograms Salmonella typhosa 0901 endotoxin. Other experimental groups included normal and sham-operation rats and animals with a unilateral nephrectomy or with one kidney rendered ischemic by complete ligature of the renal vessels and of the ureter. All the animals were sacrificed 4 hours after endotoxin, and kidney sections stained with PTAH were examined for the presence of fibrin thrombi. Glomerular thrombosis was never observed in any hydronephrotic kidney, but occurred with a low incidence (16%) in the contralateral organ in the group given endotoxin the second day after UO. The incidence and severity of glomerular capillary thrombosis gradually increased in the normal kidney as the delay between surgery and endotoxin was prolonged; the incidences (P less than 0.01) were 45% and 83%, respectively, after 6 and 10 days. Endotoxin failed totally to initiate the lesion 1 day after UO as well as in normal, sham-operation and unilaterally nephrectomized rats, and in animals with combined UO and ligature of the renal circulation. We conclude that the perfused hydronephrotic kidney liberates a factor(s) that sensitizes to DIC and glomerular thrombosis, typical of the generalized Shwartzman reaction.