Manabu Ishihara1, Nobuto Nakanishi2, Rie Tsutsumi3, Kanako Hara3, Kyoka Machida3, Nobuaki Yamamoto4, Yasuhisa Kanematsu1, Hiroshi Sakaue3, Jun Oto5, Yasushi Takagi1. 1. Department of Neurosurgery, Institute of Biomedical Sciences, Tokushima University, 2-50-1 Kuramoto, Tokushima 770-8503, Japan. 2. Emergency and Critical Care Medicine, Tokushima University Hospital, 2-50-1 Kuramoto, Tokushima 770-8503, Japan. Electronic address: nakanishi.nobuto@tokushima-u.ac.jp. 3. Department of Nutrition and Metabolism, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima 770-8503, Japan. 4. Department of Clinical Neuroscience, Institute of Biomedical Sciences, Tokushima University, 2-50-1 Kuramoto, Tokushima 770-8503, Japan. 5. Emergency and Critical Care Medicine, Tokushima University Hospital, 2-50-1 Kuramoto, Tokushima 770-8503, Japan.
Abstract
INTRODUCTION: Urinary titin is a biomarker of muscle atrophy, which is a serious complication after stroke. However, there are currently no clinical data regarding urinary titin in stroke patients. METHODS: Consecutive stroke patients admitted to the stroke care unit were included. Spot urine samples were collected immediately after admission, and on days 3, 5, and 7. The primary outcome was the trend of urinary titin in patients after acute stroke. The secondary outcomes included the association between the peak urinary titin level and the modified Rankin Scale (mRS) score, the National Institutes of Health Stroke Scale (NIHSS) score, and the Barthel index (BI) upon hospital discharge. Multivariate analysis was adjusted for age, sex, NIHSS at admission, and the peak urinary titin to predict poor outcome (mRS 3-6). RESULTS: Forty-one patients were included (29 male; age, 68 ± 15 years), 29 had ischemic stroke, 8 had intracerebral hemorrhage, and 4 had subarachnoid hemorrhage. The levels of urinary titin on days 1, 3, 5, and 7 were 9.9 (4.7-21.1), 16.2 (8.6-22.0), 8.9 (4.8-15.2), and 8.7 (3.6-16.2) pmol/mg Cr, respectively. The peak urinary titin level was associated with the mRS score (r = 0.55, p < 0.01), the NIHSS score (r = 0.72, p < 0.01), and the BI (r = -0.59, p < 0.01) upon hospital discharge. In multivariate analysis, the peak urinary titin was associated with poor outcome (p = 0.03). CONCLUSIONS: Urinary titin rapidly increased after stroke and was associated with impaired functional outcomes at hospital discharge.
INTRODUCTION: Urinary titin is a biomarker of muscle atrophy, which is a serious complication after stroke. However, there are currently no clinical data regarding urinary titin in strokepatients. METHODS: Consecutive strokepatients admitted to the stroke care unit were included. Spot urine samples were collected immediately after admission, and on days 3, 5, and 7. The primary outcome was the trend of urinary titin in patients after acute stroke. The secondary outcomes included the association between the peak urinary titin level and the modified Rankin Scale (mRS) score, the National Institutes of Health Stroke Scale (NIHSS) score, and the Barthel index (BI) upon hospital discharge. Multivariate analysis was adjusted for age, sex, NIHSS at admission, and the peak urinary titin to predict poor outcome (mRS 3-6). RESULTS: Forty-one patients were included (29 male; age, 68 ± 15 years), 29 had ischemic stroke, 8 had intracerebral hemorrhage, and 4 had subarachnoid hemorrhage. The levels of urinary titin on days 1, 3, 5, and 7 were 9.9 (4.7-21.1), 16.2 (8.6-22.0), 8.9 (4.8-15.2), and 8.7 (3.6-16.2) pmol/mg Cr, respectively. The peak urinary titin level was associated with the mRS score (r = 0.55, p < 0.01), the NIHSS score (r = 0.72, p < 0.01), and the BI (r = -0.59, p < 0.01) upon hospital discharge. In multivariate analysis, the peak urinary titin was associated with poor outcome (p = 0.03). CONCLUSIONS: Urinary titin rapidly increased after stroke and was associated with impaired functional outcomes at hospital discharge.