Rhabdomyolysis, the disintegration of striated muscle, results in the leakage of muscle constituents into the extracellular space, with subsequent reabsorption into the circulation. It ranges from asymptomatic illness to a life-threatening condition associated with acute renal failure (ARF).
Creatine kinase (CK) and myoglobin (Mb) are both markers of muscular damage in rhabdomyolysis. Whereas Mb is considered the principal compound causing tubular damage, the serum-CK level is presently guiding therapeutic interventions. In association with myocardial infarction, Mb has been found to disappear from the blood faster than CK. Considering its etiological role this suggests that serum-Mb levels, rather than that of CK, should be used to guide prophylaxis and therapy in patients with rhabdomyolysis and ARF. There is no clear agreement about whether any laboratory measures provide prognostic information indicating the development of ARF.
Removal of myoglobin by hemofiltration has been recommended, but its effects on ARF in rhabdomyolysis remain to be proven, and the elimination kinetics of myoglobin is poorly understood.
The conclusions of existing studies must be viewed with caution because of the large variations in study design and selection bias and the small number of subjects studied. There is a need for further studies that compare the values of myoglobin and CK in blood of this group of patients. This review of the literature aims to summarise current understanding of relation changes in concentration of myoglobin and kreatine kinase blood samples from of patients requiring treatment for traumatic, ischemic or postoperative rhabdomyolysis.