Uptake of indium-111-labeled platelets and indium-111 oxine by murine kidneys after total-body irradiation.

Radiation nephropathy is a well-known late manifestation of renal irradiation in human beings and experimental animals. Its pathogenesis is unclear, but vascular injury may play a role. Endothelial cells have been demonstrated to manifest a variety of abnormalities within hours of exposure to radiation. In the present experiments mice were exposed to lethal doses of whole-body radiation, and the distribution of 111In-labeled platelets was evaluated during the first week after irradiation. The purpose was to determine if early abnormalities of endothelial cells would be manifested by altered sequestration of platelets in kidneys and other organs. It was found that the indium accumulated in the kidneys of irradiated mice to a greater extent than in nonirradiated mice, supporting the possibility of early vascular injury. In control experiments, administration of 111In-oxine was also followed by excessive accumulation of radioactivity in kidneys of irradiated mice, but the pattern of accumulation differed from that seen after injection of radiolabeled platelets. Renal hyperemia was not demonstrable with 51Cr-labeled red cells, renal vascular permeability was not detected with 125I-labeled albumin, and the pattern of renal uptake of plasma proteins labeled with 59Fe or 111In did not coincide with that seen from 111In administered as labeled platelets or oxine. Renal uptake of 111In-oxine was not associated with alterations in urinary or fecal excretion or an increase in total-body retention of the radioisotope. The findings are consistent with the notion that renal vascular injury at the time of irradiation results in accumulation of platelets or platelet constituents during the first week after total-body irradiation of mice.