The liberation of myoglobin pigment from striated muscle and its subsequent appearance in the urine is a dramatic, potentially serious, and fortunately rather rare occurrence. Many types of traumatizing damage to muscle fibers may cause a partial or complete dissolution of the muscle sarcoplasm with the release of myoglobin and probably many other of the intracellular components. Some of these substances enter the circulation, and myoglobin, at least, is excreted by the kidney. Hence, myoglobinuria is not associated specifically with any single disease process but is a sign of severe damage to a significant mass of striated muscle.
In addition to the traumatic myopathies, there have been reported a number of cases of myoglobinuria, usually recurrent and unassociated with any traumatic or toxic event. About one-third of these have been associated with muscular dystrophy. The remainder of the cases, 20 in number, have been idiopathic and unassociated with any specific
PEARSON CM, BECK WS, BLAHD WH. Idiopathic Paroxysmal Myoglobinuria: Detailed Study of a Case Including Radioisotope and Serum Enzyme Evaluations. AMA Arch Intern Med. 1957;99(3):376–389. doi:10.1001/archinte.1957.00260030056006
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