Abstract
Abnormal liver function tests are commonly observed with rhabdomyolysis, but the nature of this association is not fully defined. This study aims to determine the functional relationship between serum creatine kinase, as a marker of rhabdomyolysis severity, and liver biochemistry. We used linear regression to model the relationship between liver biochemistry and peak serum creatine kinase. A total of 528 patients with a median age of 74 years were included. The distribution of creatine kinase, bilirubin, alkaline phosphatase, alanine aminotransferase, and γ-glutamyl transferase were significantly skewed, and these variables were log-transformed prior to regression. There was a positive linear correlation between log-alanine aminotransferase and log-creatine kinase. In the multiple regression analysis, log-creatine kinase, age, acute kidney injury stage, and chronic liver disease were independently associated with log-alanine aminotransferase. This model explained 46% of the variance of log-alanine aminotransferase. We found no correlation between the log-creatine kinase and the log-bilirubin, log-alkaline phosphatase, or log-γ-glutamyl transferase. Serum alanine aminotransferase was not associated with inpatient mortality but a higher creatine kinase-alanine aminotransferase ratio was associated with lower odds of mortality. In conclusion, an isolated elevation in alanine aminotransferase can occur in rhabdomyolysis, and it may be possible to anticipate the level of increase based on the peak creatine kinase.
Highlights
Rhabdomyolysis is a syndrome of skeletal muscle injury
This study was based on a patient cohort which we have previously examined for acute kidney injury (AKI) outcomes [15], and the patients included in this current study represented a subset of that cohort
From the standardized coefficients (β), we showed that log pCK had a strong effect size on log ALT but AKI stage, age, and chronic liver disease only had a weak effect
Summary
Rhabdomyolysis is a syndrome of skeletal muscle injury. Severe cases may present with muscular pain and weakness, brown discoloration of urine, compartment syndrome, and disseminated intravascular coagulation. The breakdown of muscle results in the release of cellular contents into the circulation, which are responsible for the systemic complications. Excess amounts of potassium and phosphate, along with hypocalcemia from calcium sequestration, contribute to the risk of cardiac arrhythmias. Myoglobin released from muscle can cause vasoconstriction, tubular casts, and oxidative stress in the kidney, resulting in acute kidney injury (AKI). A number of enzymes are released including creatine kinase (CK), lactate dehydrogenase, and aldolase [1]. Rhabdomyolysis is due to diverse causes that are inherited or acquired. Acquired causes are more common and include
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