The marked radiosensitivity of renal tissue represents a limitation on the total radiotherapeutic dose that safely can be applied to treatment volumes that include the kidneys. Radiation nephropathy is characterized by a progressive reduction in renal hemodynamics associated with a severe anemia. The latter is often normochromic normocytic in character, but can progress to a microangiopathic hemolytic anemia. The pathogenic mechanisms responsible for the development of radiation nephropathy remain ill-defined. Experimental studies which allow serial determinations of functional, morphologic, and cell kinetic radiation-induced changes indicate that primarily glomerular but also tubular alterations occur in the primary stages of radiation nephropathy. Glomerular capillary endothelial cell loss is seen within several weeks of irradiation. Remaining endothelial cells exhibit increased permeability leading to a subendothelial transudate. Mesangiolysis also is observed. In contrast, podocytes appear to be relatively unaffected at this stage. The endothelial changes appear to resolve, but the mesangial lesions progress, with hypercellularity and/or hypertrophy, increased mesangial matrix, mesangial sclerosis, and ultimately, glomerulosclerosis. These mesangial changes are similar to those observed in other chronic glomerulopathies. Dietary protein restriction, corticosteroids, and ACE-inhibitors all can reduce the severity of experimental radiation nephropathy.
Robbins, M. E. C. and Bonsib, S. M.
"Radiation Nephropathy: A Review,"
Scanning Microscopy: Vol. 9
, Article 22.
Available at: https://digitalcommons.usu.edu/microscopy/vol9/iss2/22