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Chronic obstructive pulmonary disease (COPD) is a respiratory disorder characterized by persistent airflow limitation and is increasingly recognized as a systemic disease accompanied by reduced physical function and activity. Frailty is prevalent in patients with COPD and is associated with adverse outcomes, including falls, hospitalization, and mortality. However, frailty assessment in clinical practice largely depends on functional measures such as gait speed and grip strength, so sufficient objective and quantitative biomarkers are not established.
The urinary N-terminal Titin fragment (N-Titin) has recently been attracting attention as a noninvasive biomarker reflecting skeletal muscle damage. However, the association with frailty in COPD has not been fully revealed.

A research group led by Dr. Fumiya Kotajima and Dr. Takeshi Hisada at the Department of Rehabilitation Sciences, Gunma University Graduate School of Health Sciences, conducted a cross-sectional observational study involving 50 stable outpatients (27 with COPD and 23 with asthma) to investigate whether urinary N-Titin is associated with frailty in COPD.
Physical frailty was assessed according to the Japanese version of the Cardiovascular Health Study (J-CHS) criteria. Urinary N-Titin levels were measured by an enzyme-linked immunosorbent assay and expressed as the N-Titin-to-Creatinine ratio (N-Titin/Cr). Associations between N-Titin/Cr and clinical parameters, including forced expiratory volume in 1 second (FEV₁), walking speed, and serum creatine kinase (CK), were evaluated by correlation and multivariable analyses. Receiver operating characteristic (ROC) analysis was performed to assess its ability to discriminate frailty.

Key Findings
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N-Titin/Cr was significantly higher in patients with COPD than in those with asthma
(median 7.6 vs. 4.7 pmol/mg Cr, p = 0.001), whereas CK levels did not differ significantly

In COPD, N-Titin/Cr was significantly higher in the frail group than in the non-frail group
(median 15.9 vs. 7.0 pmol/mg Cr, p = 0.037), while no such association was observed in asthma

N-Titin/Cr was positively correlated with J-CHS score and negatively correlated with walking speed and FEV₁, indicating associations with frailty status, physical performance, and pulmonary function

Multivariable analysis demonstrated that N-Titin/Cr was independently associated with J-CHS score (β = 4.38, p = 0.004)

ROC analysis showed a moderate ability to discriminate frailty (AUC = 0.75; cutoff 14.3 pmol/mg Cr; specificity 94.4%, sensitivity 55.6%)
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These findings suggest that urinary N-Titin/Cr is associated with frailty in COPD and may reflect skeletal muscle damage. Skeletal muscle dysfunction in COPD is characterized by muscle wasting and activation of proteolytic pathways, including the ubiquitin–proteasome system, potentially leading to Titin degradation and increased urinary excretion of N-Titin.

Urinary N-Titin/Cr is a noninvasive and quantitative biomarker that may capture chronic muscle injury, which conventional markers such as CK is not able to detect. It may serve as a supplementary biomarker for frailty assessment in COPD, complementing established tools such as the J-CHS criteria.

Further longitudinal studies will be required to determine its utility in monitoring changes in muscle status during interventions such as pulmonary rehabilitation and nutritional support.


Please refer to the following publication for more details.

Fumiya Kotajima et al.
Urinary N-terminal titin fragment as a supplementary marker for frailty in chronic obstructive pulmonary disease
Respir Investig. 2026; 64(4):101445.


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