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In 1941, during the London bombardment, British physician Eric Bywaters studied bombing victims who developed kidney failure due to crushed limbs, leading to the identification of "crush syndrome." He noted dark brown casts in urine and renal tubules containing brown pigment. Ironically, Bywaters was rejected from military service due to a kidney issue. By 1944, he demonstrated that the leakage of muscle contents into circulation, caused by ischemia and reperfusion, led to renal failure, coining the term rhabdomyolysis (RM). This condition can arise from various causes, including trauma, exertion, infections, and metabolic disorders, with a significant risk of acute renal failure (ARF). Despite nearly 70 years since Bywaters' observations, the molecular mechanisms behind this pathology remain poorly understood, necessitating further research into renal damage and potential treatments. Historically, renal vasoconstriction and heme protein-induced cytotoxicity have been identified as key factors in RM-induced renal failure, leading to various treatment attempts with limited success. Recent studies emphasize oxidative injury's role in this condition. This research investigates myoglobin-mediated oxidative stress using in vitro and in vivo models, testing iron chelators and antioxidants to inhibit oxidative stress and correlate findings with renal protection. The insights gained may enhance understanding of the molecular processes
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Therapeutic approaches to minimise acute renal failure in an animal model of myoglobinuria, Ludwig K. Gröbler
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- Erscheinungsdatum
- 2013
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