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Serum myoglobin immunoassays: obsolete or still clinically useful?

Rhabdomyolysis is conventionally defined as a clinical syndrome attributable to massive skeletal muscle injury, with consequent leakage of many intracellular and often toxic components (e.g. potassium and myoglobin among others) into the blood. The epidemiologic data attests that rhabdomyolysis is a relatively frequent condition in the adult populations, with as many as 26,000 cases annually reported in the US [1]. The most frequent causes of rhabdomyolysis include traumatic muscle injury, hereditary enzyme disorders, drugs, toxins, endocrinopathies, malignant hyperthermia, neuroleptic malignant syndrome, heatstroke, hypothermia, severe electrolyte disorders, diabetic ketoacidosis, severe hyperthyroidism, as well as bacterial or viral infections [2]. Although the overall mortality for rhabdomyolysis depends on many factors such as the etiology, comorbid conditions and complications, the death rate remains high, comprised between 5% and 10%. Notably, the most frequent and severe complication of rhabdomyolysis is acute kidney injury (AKI), the presence of which contributes to enhancing the overall mortality up to 30%, approximating 60% in intensive care unit (ICU) patients [3]. The diagnosis of rhabdomyolysis is prevalently based on clinical and laboratory data. For decades the laboratory diagnostics of rhabdomyolysis has been essentially based on the assessment of the enzymatic activity of creatine kinase (CK; EC 2.7.3.2), which has since been regarded as the most sensitive and predictive biomarker in patients with this condition. The measurement of urinary myoglobin, an additional biomarker of muscle damage, has been gradually abandoned due to the many clinical and technical issues related to its analytical assessment [4, 5]. After a decade of magnificence, the measurement of serum myoglobin has also been progressively forsaken in clinical laboratories, due to the introduction of more sensitive cardiospecific troponin immunoassays, which have made the assessment of myoglobin virtually useless for diagnosing acute coronary syndrome [6]. Nevertheless, evidence which has merged over the past 5 years attests that the measurement of myoglobin in serum (or plasma) may still have an important role in patients with rhabdomyolysis, especially for predicting the development of AKI. Nearly 5 years ago, Kasaoka et al. studied 30 patients with rhabdomyolysis (the leading causes were trauma, burns and ischemia), 12 of whom developed AKI [7]. In multivariate logistic regression analysis, the peak value of serum myoglobin was found to be a much better predictor of AKI [odds ratio (OR), 1.19; 95% confidence interval (CI), 0.99–1.43] than the peak value of CK (OR, 0.99; 95% CI, 0.92–1.06). The overall diagnostic performance of serum myoglobin was noteworthy [i.e. exhibiting an area under the curve (AUC) of ~0.90]. El-Abdellati et al. retrospectively studied 1769 adult ICU patients, using hemodialysis and mortality as outcome variables [8]. The risk for the onset of AKI was found to be the highest for serum myoglobin (OR, 7.87; 95% CI, 4.60–13.85; p < 0.001), followed by CK (OR, 2.21; 95% CI, 1.45–3.38; p < 0.001) and urinary myoglobin (OR, 1.61; 95% CI, 1.21–2.13; p = 0.001). Serum myoglobin was found to be the best predictor of AKI development (AUC, 0.790), whereas the efficiency of CK (AUC, 0.759) was also preceded by that of urinary myoglobin (AUC, 0.766). Two additional and important aspects were highlighted in this study. First, elevated CK values with concomitant normal serum myoglobin concentration were not predictive of AKI (p = 0.882). Then, the peak of CK values (72±145 h) was reached significantly later than that of both serum (30±87 h) and urinary (33±77 h) myoglobin. Premru et al. studied the incidence of myoglobinuric AKI and the need for hemodialysis in 484 patients with suspected rhabdomyolysis [9]. The value of CK significantly correlated with the severity of rhabdomyolysis, but such a correlation was absent in patients with myoglobinuric AKI. More specifically, a better association was found between serum creatinine and serum myoglobin (r = 0.33; p < 0.001) than between serum creatinine and CK (r = 0.15; p = 0.01). Interestingly, when patients were grouped by CK