Myoglobinuria pathophysiology

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Normally myoglobin is filtered and excreted with the urine, but if too much myoglobin is released into the circulation from damaged muscle tissue (rhabdomyolysis), which has very high concentrations of myoglobin, it can be toxic to the renal tubular epithelium and so may cause acute kidney injury.[1] It is not the myoglobin itself that is toxic (it is a protoxin) but the ferrihemate portion that is dissociated from myoglobin in acidic environments (e.g., acidic urine, lysosomes).

Myoglobin is a sensitive marker for muscle injury, making it a potential marker for myocardial infarction in patients with chest pain.[2] However, elevated myoglobin has low specificity for acute myocardial infarction (AMI) and thus CK-MB, cardiac Troponin, ECG, and clinical signs should be taken into account to make the diagnosis.

References

  1. Naka T, Jones D, Baldwin I, Fealy N, Bates S, Goehl H, Morgera S, Neumayer HH, Bellomo R (Apr 2005). "Myoglobin clearance by super high-flux hemofiltration in a case of severe rhabdomyolysis: a case report". Critical Care. 9 (2): R90–5. doi:10.1186/cc3034. PMC 1175920. PMID 15774055.
  2. Weber M, Rau M, Madlener K, Elsaesser A, Bankovic D, Mitrovic V, Hamm C (Nov 2005). "Diagnostic utility of new immunoassays for the cardiac markers cTnI, myoglobin and CK-MB mass". Clinical Biochemistry. 38 (11): 1027–30. doi:10.1016/j.clinbiochem.2005.07.011. PMID 16125162.

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