A case of multiple organ failure induced by postoperative radiation therapy probably evoking oxidative stress

• Published in: Nihon Jinzo Gakkai shi Vol. 37; no. 1; pp. 81 - 85
• Main Authors: SOEJIMA, Akinori, ISHIZUKA, Shynji, SUZUKI, Michihiko, MINOSHIMA, Shinobu, NAKABAYASHI, Kimimasa, KITAMOTO, Kiyoshi, NAGASAWA, Toshihiko
• Format: Journal Article
• Language: Japanese
• Published: Japan Japanese Society of Nephrology 1995
• Subjects: chronic renal failure, radiation therapy, oxidative stress, multiple organ failure; Female; Humans; Kidney Failure, Chronic - etiology; Kidney Failure, Chronic - metabolism; Middle Aged; Multiple Organ Failure - etiology; Multiple Organ Failure - metabolism; Oxidative Stress; Radiation Injuries - etiology; Radiation Injuries - metabolism; Radiotherapy - adverse effects; Rectal Neoplasms - radiotherapy; Rectal Neoplasms - surgery
• ISSN: 0385-2385; 1884-0728
• DOI: 10.14842/jpnjnephrol1959.37.81

In recent years, several laboratories have suggested that serum levels of antioxidant activity and redox balance are reduced in patients with chronic renal failure. Some clinical reports have also proposed that defective serum antioxidative enzymes may contribute to a certain uremic toxicity through peroxidative cell damage. A 48-year-old woman was referred to us from the surgical department of our hospital because of consciousness disturbance, panctytopenia and acute acceleration of chronic azotemia after postoperative radiation therapy. We diagnosed acute acceleration of chronic renal failure with severe acidemia and started hemodialysis therapy immediately. Two days after admission to our department, she developed upper abdominal sharp pain and bradyarrhythmia. Serum amylase activity was elevated markedly and the ECG finding showed myocardial ischemia. On the 24th hospital day these complications were treated successfully with conservative therapy and hemodialysis. We considered that radiation therapy in this patient with chronic renal failure evoked marked oxidative stress and that deficency of transferrin played an important role in peroxidative cell damage.