Biochip Array Profiling of Neuron Specific Enolase, Neutrophil Gelatinase‐associated Lipocalin, Soluble Tumor Necrosis Factor Receptor I, D‐Dimer, Thrombomodulin, and C‐reactive Protein in End Stage Renal Disease

Abstract

Plasma samples from 39 patients with clinically confirmed end‐stage renal disease (ESRD) were collected prior to a maintenance hemodialysis. A pilot group of ten normal individuals, both male and female, were included as control. Cerebral Array II chips were used in the Randox® system to simultaneously measure Neuron Specific Enolase (NSE), Neutrophil Gelatinase‐associated Lipocalin (NGAL), Soluble Tumor Necrosis Factor Receptor I (TNFRI), D‐Dimer (DD), Thrombomodulin (TM), and C‐reactive protein (CRP). As compared to normals, all markers studied showed an upregulation in ESRD patients. Most notably TNFRI showed a 25 fold increase in patients with ESRD (mean 7.4 ± 2.4, range 3.1 to 13.6) compared to the control (mean 0.3 ± 0.1, range 0.2 to 0.5). TM showed a 6.6 fold increase (mean 7.0 ± 2.5, range 2.5 to 14.1) compared to control (mean 1.1 ± 0.2, range 0.8 to 1.4), and NGAL showed a 5.5 fold increase (mean 1416 ± 203, range 839 to 1729), compared to control (mean 257 ± 74, range 115 to 377). Increases in CRP and DD were also noted up to 2.8 fold. These studies show that some newer markers such as TNFRI, NGAL and NSE are upregulated in ESRD. However, the clinical significance of these markers still needs to be further explored. In addition, this study validates the role of endothelial damage and endogenous thrombotic processes in ESRD as evidenced by the increased levels of thrombomodulin and D‐Dimer.