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Thank you for attending THSNA 2026. The virtual meeting is now closed.
Thank you for attending THSNA 2026. The virtual meeting is now closed.
Presentation Details
| Evaluation of Plasminogen Activator Inhibitor-1 in End-Stage Renal Disease Patients Riddhi Surve1, Charvi Chegireddy1, Fakiha Siddiqui 2, Jawed Fareed2, Vinod Bansal2. 1Global Thrombosis Forum, Suwanee, GA, USA.2Loyola University, Maywood, IL, USA |
Abstract
Background: Fibrinolysis, the physiological process that dissolves fibrin clots through the activation of plasmin, maintains vascular patency and prevents excessive thrombosis. Plasminogen Activator Inhibitor-1 (PAI-1) is the principal inhibitor of this system; its overproduction leads to a hypofibrinolytic, pro-thrombotic state. In End-Stage Renal Disease (ESRD), defined by a glomerular filtration rate of <15 mL/min/1.73 m², patients suffer from systemic inflammation, oxidative stress, and endothelial dysfunction. These conditions upregulate PAI-1 expression in endothelial and mesangial cells, promoting vascular fibrosis and thrombosis. Understanding PAI-1 dysregulation in ESRD is essential for identifying patients with fibrinolytic imbalance and elevated cardiovascular risk. Objectives: This study aimed to quantitatively assess PAI-1 plasma concentrations in ESRD patients compared with healthy individuals and to determine whether elevated PAI-1 levels indicate a persistent fibrinolytic deficit contributing to thrombo-inflammation. We hypothesized that PAI-1 concentrations would be significantly elevated in ESRD patients and might vary by vascular access type. Methods: A prospective cohort of 72 ESRD patients undergoing hemodialysis and 50 age-matched healthy controls was examined. All samples originated from the Loyola University Chicago biobank, where blood was drawn into 3.2 % sodium citrate tubes, double-centrifuged to obtain platelet-poor plasma, and stored at −80 °C until analysis. PAI-1 antigen levels were quantified using a Sandwich ELISA (Molecular Innovations Inc.) according to the manufacturer's protocols. Data were assessed for normality and analyzed using nonparametric tests: the Mann–Whitney U test compared the ESRD and control groups, and Spearman's correlation explored relationships between PAI-1 and secondary inflammatory indices (CRP, D-dimer), with significance defined as p <0.05. Visualization included a scatterplot illustrating PAI-1 distributions between ESRD and control cohorts (Figure 1). Results (Figure 1): ESRD patients showed markedly different PAI-1 distributions compared with healthy controls. Median PAI-1 levels were 7.587 ng/mL (IQR: 4.031–18.29) in ESRD and 23.74 ng/mL (IQR: 8.338–30.45) in controls. Despite the lower median, the ESRD group demonstrated greater variability, with a wider range (0.477–67.54 ng/mL) and a higher standard deviation, suggesting heterogeneous fibrinolytic impairment. A Mann-Whitney test confirmed a significant difference between groups (p <0.0001). These findings highlight substantial dysregulation of PAI-1 in ESRD patients, consistent with endothelial injury and reduced fibrinolytic capacity. Conclusions: PAI-1 levels in ESRD patients exhibit significant differences in distribution and greater variability than in healthy controls, reflecting disrupted fibrinolysis and endothelial stress. These findings support PAI-1 as a relevant biomarker of thrombo-inflammatory imbalance in ESRD. Incorporating PAI-1 measurement into clinical evaluation may help identify patients at increased risk of vascular complications. Further study, including longitudinal monitoring and correlations with dialysis factors, may clarify its utility as a diagnostic and therapeutic marker.
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No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.