Reversible inner medullary vascular obstruction in acute experimental hydronephrosis.

The pathogenesis of experimental unilateral hydronephrosis was studied in the rat, with emphasis on the role of medullary vascular obstruction. The medullary circulation was evaluated after increasing periods of ureteral obstruction (up to 48 hours) using in vivo perfusion of silicone rubber or colloidal carbon. Evidence of inner medullary hypoperfusion was seen after 1 hour, and by 6 hours, the entire papilla was ischemic. Papillar hypoperfusion was still present at 24 and 48 hours, but significant recirculation occurred in the presence of continued obstruction. Release of ureteral obstruction caused rapid reversal of the perfusion defect. Histologic studies of the renal parenchyma adjacent to the pelvis showed increasing vascular congestion, focal interstitial edema, and extravasation of erythrocytes; these changes were also diminished after release of obstruction. Endothelial swelling or thrombosis in inner medullary blood vessels was not observed. Inner medullary tubules showed degenerative changes in kidneys that had been obstructed for 6 hours or more; at later periods (18 hours or more) focal necrosis was seen, but it never involved the entire papilla. Thus, reversible collapse of inner medullary blood vessels occurs in acute unilateral hydronephrosis and may provide the basis for the development of ischemic tubular damage. The findings suggest that the vascular obstruction may be due to increased intrapelvic pressure, rather than endothelial swelling or thrombosis. The vascular-tubular defect may be relevant to the altered medullary physiology observed in this condition.