Procalcitonin Elevation in Intoxication- and Immobilization-Related Non-Traumatic Rhabdomyolysis: Association with Muscle Injury Severity and Renal Dysfunction

Background: Procalcitonin (PCT) is widely used as a biomarker of bacterial infection, but it may also increase in non-infectious inflammatory states. This study investigated the association of PCT with muscle injury severity and renal dysfunction in patients with non-traumatic rhabdomyolysis. Methods: We prospectively enrolled 39 adults with non-traumatic rhabdomyolysis (n = 39). Admission and longitudinal laboratory data included creatine kinase (CK), myoglobin, PCT, C-reactive protein (CRP), creatinine, and urea. Associations were assessed using Spearman correlation analysis with false-discovery-rate correction for multiple comparisons. Independent predictors of admission PCT were evaluated using linear regression with PCT (log10) as the dependent variable. Longitudinal dynamics were analyzed using linear mixed-effects models and a generalized mixed-effects sensitivity model. Results: At admission, after false-discovery-rate correction, PCT remained positively correlated with creatinine, CK, urea, and CRP; the weaker correlation with myoglobin did not remain significant after correction. In the primary admission model, both creatinine (log10) and CK (log10) were independently associated with PCT (log10), whereas infection status was not. In the broader sensitivity model, only creatinine (log10) remained significant. Longitudinal analyses showed that CK (log10) remained independently associated with PCT over time, including in the gamma mixed-effects sensitivity model; in that model, infection status was not independently associated with PCT. Conclusions: In this exploratory single-centre cohort of patients with predominantly intoxication- or immobilization-related “found-down” non-traumatic rhabdomyolysis, PCT elevation was associated with markers of muscle injury and renal dysfunction. Infection status was not independently associated with PCT in the fitted models; however, the modest sample size means that smaller infection-related effects cannot be excluded. These findings should therefore be interpreted cautiously and require confirmation in larger, more etiologically diverse rhabdomyolysis cohorts.