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Introduction: Chronic kidney disease (CKD) is associated with high risk of cardiovascular disease (CVD), independent of established cardiovascular risk factors, with cystatin C (cysC) demonstrating associations with CVD independent of creatinine-based kidney function. We tested the association between reduced kidney function (eGFR, cysC) and kidney damage (albuminuria) and intracranial atherosclerotic disease (ICAD) by vessel wall MRI (VWMRI) in the ARIC-Neurocognitive (ARIC-NCS) study.Methods: In this cross-sectional analysis, we sampled ARIC participants with kidney function measurements who completed intracranial VWMRI/MRA. eGFR was estimated by both creatinine and cysC(eGFRcr-cys). Albuminuria was assessed as urinary albumin-creatinine ratio (ACR). Presence and number of intracranial plaques and presence of ≥50% stenosis for individuals with plaques were considered as outcomes in separate multivariable binomial and multinomial logistic models, with adjustment for sociodemographic features, established cardiovascular risk factors, C-reactive protein, and use of antithrombotic and lipid lowering agents.Results: 1762 participants (age 76.5±5.3) with interpretable MRI and kidney function measurements were included. eGFRcr-cys<60 ml/min/1.73 m2 (vs≥ 60) was associated with plaque presence(adjusted OR 1.33, 95%CI 1.05-1.68). A similar association between ACR or cysC and plaque presence lost significance in adjusted models (ACR≥30 vs <10: OR 1.19, 95% CI 0.89-1.60; CysC: OR 1.19 for increase by 1 mg/L, 95% CI 0.78-1.82). In adjusted models, compared with eGFRcr-cys≥60 ml/min/1.73 m2, participants with eGFRcr-cys<60 had an OR of 1.47 (95% CI 1.1-1.96) for having 1 vs zero plaque, and an OR of 1.23 (95% CI 0.93-1.63) for having ≥2 vs zero plaques. eGFRcr-cys, CysC or ACR were not associated with ≥50% stenosis among those with plaques.Conclusion: In older adults in the ARIC study, reduced kidney function measured by eGFRcr-cys was independently associated with ICAD burden. The potential mechanism is unknown but may be mediated by decreased clearance of metabolic toxins or proinflammatory cytokines that may play roles in the pathogenesis of atherosclerosis. This finding may help to better identify a high risk population for ICAD.