To evaluate the frequency and etiology of elevated creatine kinase (CK) in patients with peripheral neuropathy.

CK catalyzes the conversion of creatinine to phosphocreatine and plays a pivotal role in providing ATP needed for muscle contraction. CK is a nonspecific marker for muscle damage and commonly elevated in muscle and motor neuron disorders. CK elevation in peripheral neuropathy is less well described but has been reported in chronic inflammatory demyelinating neuropathy and anecdotally in inherited neuropathies such as Charcot-Marie-Tooth disease. This prior work suggests elevated CK could also be associated with other neuropathies, a finding not yet shown in the literature.

We performed a retrospective chart review of clinically confirmed peripheral neuropathies evaluated in the Ohio State University’s neuromuscular clinic over a 5-year period. Patient’s 18 and older were included in the study. Demographic data, clinical history, physical examination, EMG, and laboratory data were analyzed. Elevated CK was defined as > 184U/L in females, and >220U/L in males.

A total of 497 patients (253 men, 244 women, mean age 58 years ± 14) with peripheral neuropathy and CK drawn were identified, and 85 (17.1%) had elevated CK. A total of 53 patients were found to have concomitant etiology, including myopathy, motor neuron disease, statin use, African race, or chronic kidney disease but 30 patients, representing 6.0% of our total peripheral neuropathy cohort, had no other identifiable etiology. The majority of cases without an identified concomitant etiology had hereditary and idiopathic neuropathies. Median CK elevation in this group was 293.

Modest CK elevation can be found in a significant percentage of peripheral neuropathy patients without another identifiable etiology. Recognition of such a finding can help guide evaluation and management decisions.