ArticleInternational journal of general medicine2025
Serum Cystatin C and 90-Day Neurological Functional Prognosis in Acute Ischemic Stroke: Insights from a Prospective Cohort and Mendelian Randomization.
Article in International journal of general medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The relationship between cystatin C levels and 90-day neurological functional prognosis in acute ischemic stroke (AIS) is not fully understood. This study investigated this association prospectively and employed Mendelian randomization (MR) analysis to assess potential causality. Methods: A prospective cohort study enrolled 786 patients with AIS admitted to a tertiary Stroke Center between 2021 and 2023. Serum cystatin C levels were measured within 48 hours of admission. Associations with adverse 90-day neurological functional outcome (modified Rankin Scale score > 2) were assessed using univariate and multivariable logistic regression. Cox regression models evaluated all-cause mortality during long-term follow-up. Mediation analysis examined the role of inflammatory mediators (Monocyte-to-Lymphocyte Ratio [MLR], Neutrophil-to-Lymphocyte Ratio [NLR], Systemic Inflammatory Response Index [SIRI], Systemic Immune-Inflammation Index [SII]) in the cohort. Causality was further evaluated using a two-sample MR approach with genetic instruments to infer the effect of cystatin C on ischemic stroke risk. Results: Elevated cystatin C levels were independently associated with higher odds of adverse 90-day functional outcome (adjusted odds ratio [OR] = 2.13, 95% CI: 1.34-3.38, p=0.001) and increased mortality risk (adjusted hazard ratio [HR] = 1.97, 95% CI: 1.09-3.54, p=0.024). Mediation analysis identified systemic inflammation markers as significant mediators, accounting for 16.1% to 20.2% of the total effect of cystatin C on adverse prognosis. MR analysis provided evidence supporting a causal relationship, indicating that genetically predicted higher cystatin C levels were associated with an increased risk of ischemic stroke (OR = 1.10, 95% CI: 1.02-1.18, p=0.011). Conclusion: Elevated cystatin C levels demonstrated a significant association with worse 90-day functional outcome and higher mortality in these patients, partially mediated through systemic inflammation. MR findings suggested a potential causal role of cystatin C in ischemic stroke pathogenesis. Cystatin C may represent a valuable integrated biomarker for both prognosticating outcomes in AIS and predicting ischemic stroke risk.
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