Abstract:Objective To explore the correlation between cystatin C and early neurological deterioration( END) in elderly patients with acute ischemic stroke( AIS). Methods A total of 140 patients with AIS aged over 60 treated in People's Hospital of Xinjiang Uygur Autonomous Region from December 2017 to May 2018 were selected. According to the level of serum cystatin C, patients were divided into 2 groups, 45 in the low-level group and 95 in the high-level group. The patients were divided into END group (53 cases) and NEND group( 87 cases without END) according to the National Institutes of Health Stroke Scale (NIHSS). The relationship between clinical data and END was compared. Results Hypertension, coronary heart disease, atrial fibrillation, large atherosclerosis( LAA), number of atherosclerotic plaques, incidence of END, infection and C-reactive protein( CRP) values in high-level group were higher than those in low-level group, while the number of small vessel occlusion( SVO) and uric acid values were lower than those in lowlevel group, and the differences were statistically significant( P< 0.05). The history of atrial fibrillation, the number of cardiogenic embolism( CE), cystatin C, white blood cell count, microalbuminuria, homocysteine, fibrinogen, NIHSS score at admission, the incidence of atherosclerotic plaque and infection rate in END group were higher than those in NEND group, while SVO and triglyceride( TG) were lower than those in NEND group, and the differences were statistically significant( P < 0.05). Logistic regression analysis showed that cystatin C, NIHSS score at admission, incidence of infection and elevated homocysteine level were risk factors for END after AIS in the elderly. Cystatin C, NIHSS score at admission, incidence of infection and homocysteine were positively correlated with END. Conclusions In elderly patients with normal renal function, Cystatin C level is associated with early neurological deterioration after acute stroke. Cystatin C level is a valuable predictor of early neurological deterioration after acute stroke.