Radiation nephritis. Clinical manifestations and pathophysiologic mechanisms.
Radiation nephritis is both volume and dose related. Clinical experience would indicate that a minimum of one third of the renal volume needs to be excluded from nephrotoxic doses which appears to have a threshold of 2,000 cGy. The site of damage leading to renal failure appears to be the microvasculature ultimately expressed as glomerulosclerosis. How much direct damage to the tubular system contributes to this process is unclear, but undoubtedly the resultant systemic physiologic effects potentiate the expression of damage in the irradiated kidney. The acute syndrome, with all the potential manifestations of renal failure, rarely presents sooner than six months and appears to have no clear prodrome, although it would seem reasonable that a subclinical syndrome consisting of abnormalities detectable by urinalysis may occur. Treatment of radiation-induced nephritis or hypertension is no different from treatment for nephritis from any other cause and should be aggressive with lifelong follow-up. Carcinogenesis is a rare late expression of radiation-induced kidney damage.
D000818:Animals; D006801:Humans; D006973:Hypertension / Q000209:etiology; D007668:Kidney / Q000098:blood supply / Q000503:physiopathology; D007680:Kidney Neoplasms / Q000209:etiology; D051379:Mice; D009393:Nephritis / Q000209:etiology*; D011832:Radiation Injuries; D011878:Radiotherapy / Q000009:adverse effects*; D013997:Time Factors