SP272
PROFILING OF NEUROVASCULAR DISEASES IN PATIENTS WITH STAGE 5 CHRONIC KIDNEY DISEASE USING SPECIFIC BIOMARKER PROFILING

INTRODUCTION AND AIMS: Patients with stage 5 chronic kidney disease (CKD5D) have a higher risk for developing neurocognitive deficits. Stroke, cervical carotid artery disease (CCAD), and intracranial atherosclerosis (ICAD), are causes of such deficits in CKD5D. Chronic inflammation from renal failure increases risk for these diseases through oxidative stress and vascular dysfunction. The adverse impact on the carotid and intracranial vasculatures contributes to the multifactorial pathophysiology of neurovascular diseases. The objective is toTo profile levels of inflammatory and hemostatic biomarkers in CKD5D plasma, and relate measurements to neurovascular diagnoses.

METHODS: Eleven plasma biomarker levels in CKD5D patients (n=97) and healthy controls (n=17-50) were measured using sandwich ELISA method. Of the 97 CKD5D patients, 24 had CCAD, 19 had ICAD, and 23 had acute stroke. Data were collected in Microsoft Excel, and analyzed using GraphPad Prism. Statistics were performed with Mann-Whitney t-tests, Kruskal-Wallis non-parametric ANOVA, and non-parametric Spearman correlations.

RESULTS: Most biomarkers were elevated in CKD5D plasma, except for plasminogen activator inhibitor-1 (PAI-1; p=0.9764), compared to controls. Statistical significance was only found between CKD5D (+) and (-)CCAD inflammasomes (NALP3; p=0.0299), and between (+) and (-)stroke D-dimer (p=0.0258). Ages between each (+) and (-) disease groups were also significant (p=0.0002 CCAD; p<0.0001 ICAD; p=0.0157 stroke). D-dimer was correlated with age in CKD5D (r=0.2115, p=0.0375). Lack of difference in PAI-1 levels between CKD5D and controls could be due to the use of anticoagulants in these patients. Elevated D-dimer levels in CKD5D stroke patients could be due to increased age instead of stroke. NALP3 is known to be connected to the stability of atherosclerotic plaques in CCAD. NALP3 elevates IL-1β and IL-18, which subsequently increases risk of CCAD and stroke. Lack of more significant differences in biomarker levels between (+) and (-) disease groups could due to the BBB, which might filter out the biomarkers of our study.

CONCLUSIONS: Profiling biomarker levels of this study may be of limited value in the risk stratification of neurovascular diseases in the CKD5D population, with the possible exception of NALP3 for CCAD.