Radiation nephritis.
There is considerable similarity in the morphologic expression of radiation nephritis in man and in the rat. In both species the cellular structures as well as intercellular substances are affected. The most sensitive elements are the tubular epithelium, glomerular endothelium, the glomerular mesangium, and subendothelial and endomysial basement membranes in the arterial walls. The characteristic separation of cells from basement membranes in the glomeruli and tubules is probably due to the damage of both the cells and the membranes. Subsequent degeneration of muscle cells in the arterial media and deposition of fibrin lead to fibrinoid necrosis and thrombosis. Within the range of 1500 to 10,000 rads the nature of radiation changes remains the same irrespective of dose. Higher doses merely accelerate and aggravate the lesions and increase the frequency of severe arterial damage.
D000818:Animals; D001158:Arteries / Q000473:pathology; D001485:Basement Membrane / Q000473:pathology; D002196:Capillaries / Q000473:pathology; D006801:Humans; D007668:Kidney / Q000528:radiation effects*; D007678:Kidney Glomerulus / Q000098:blood supply / Q000473:pathology; D007684:Kidney Tubules / Q000473:pathology; D009393:Nephritis / Q000209:etiology* / Q000473:pathology; D011829:Radiation Dosage; D011832:Radiation Injuries / Q000150:complications* / Q000473:pathology; D011833:Radiation Injuries, Experimental; D051381:Rats