Increased cardiovascular events occur in ESRD patients on maintenance hemodialysis. The objective of this study was to utilize newly introduced cardiac biomarker chips and immunoenzymatic methods, profiling various biomarkers of inflammation and thrombogenesis in a defined ESRD patient population.
Blood samples from seventy two ESRD patients were drawn prior to maintenance hemodialysis. Commercially available ELISA kits for Tissue Plasminogen Activator – Plasminogen Activator Inhibitor Type-1 complex (tPA-PAI-1 complex), Plasminogen Activator Inhibitor Type-1 (PAI-1), Myeloperoxidase, (MPO), Thrombomodulin, (TM), Interleukin-1 beta (IL-1β), Anti-Annexin V, human sL-selectin, and Inter-Cellular Adhesion Molecule 1 (ICAM-1). Functional methods were used for measuring Antithrombin and Von Willebrand factor (vWF) activity were used. The biochip arrays (Randox, Evidence System, United Kingdom)for cardiac markers, included creatine kinase-MB (CK-MB), Myoglobin (Myo), Heart-type fatty acid binding protein (hFABP) and cardiac troponin I (cTn1). The cerebral array included C-reactive protein (CRP), D-Dimer (DDMER), Neuron Specific Enolase (NSE), Neutrophil Gelatinase-Associated Lipocalin (NGAL), soluble Tumor Necrosis Factor Receptor 1 (TNFRI) and Thrombodulin (TM).
ESRD patients showed assay dependent decrease in markers such as tPA-PAI-1, Anti-Annexin V, L-selectin and Antithrombin activity (ranging from 18 to 46%). The levels for MPO, TM, CK-MB, MYO, FABP, CRP, DDMER, NSE, NGAL, TNFR1, and vWF activity all showed a significant increase in the ESRD patients (ranging from 25%-5587%). No changes were observed in the IL-1B, ICAM1, or cTn1 in ESRD patients compared to normal groups.
These studies underscore the role of inflammatory and thrombotic mediators in ESRD. The cardiac biochip array revealed a remarkable elevation of the FABP and as well as a notable increase in MYO. The cerebral array revealed a remarkable elevation of the TNFR1.
No relevant conflicts of interest to declare.
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