Abstract
While ARF following rhabdomyolysis or crush syndrome is well documented, its pathophysiology has not been defined. Myoglobin, thought to be responsible for the pathogenesis of ARF, is not toxic unless dehydration or acidosis is already present. To elucidate the pathophysiology of ARF, a new experimental model was established using a crude muscle extract(ME) prepared by homo-genization of saline perfused rat thigh muscle followed by centrifugation and filtration. Experimental rats were injected i.v. with ME and control groups with saline, boiled ME, and myoglobin in normal rat serum. ME caused death at doses >10 mg ME protein/100 g and ARF at 5-10 mg. Oliguria, proteinuria, hemepigmenturia with an active urine sediment, hypocomplementemia, leucopenia and thrombocytopenia developed shortly after ME injection. These findings were not present in the control groups;transient harmless myoglobinuria was present in the control rats given myoglobin. Involvement of the coagulation system suggested by experimental data led to studies using heparin as an anticoagulant. Ten of 10 rats pretreated with heparin before ME injection lived whereas 9 of 10 controls died. This experimental model closely resembles clinical ARF secondary to rhabdomyolysis.Our data also suggest that other biological systems are activated and that muscle constituents other than myoglobin are involved in the pathogenesis of ARF following muscle injury.
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Blachar, Y., O'regan, S., Drummond, K. et al. ACUTE RENAL FAILURE (ARF) FOLLOWING EXPERIMENTAL RHABDOMYOLYSIS. Pediatr Res 11, 547 (1977). https://doi.org/10.1203/00006450-197704000-01066
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DOI: https://doi.org/10.1203/00006450-197704000-01066
