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Renal systems biology of patients with systemic inflammatory response syndrome
Journal article   Open access   Peer reviewed

Renal systems biology of patients with systemic inflammatory response syndrome

Ephraim L. Tsalik, Laurel K. Willig, Brandon J. Rice, Jennifer C. van Velkinburgh, Robert P. Mohney, Jonathan E. McDunn, Darrell L. Dinwiddie, Neil A. Miller, Eric S. Mayer, Seth W. Glickman, …
Kidney international, v 88(4), pp 804-814
01 Oct 2015
PMID: 25993322
url
https://doi.org/10.1038/ki.2015.150View
Published, Version of Record (VoR) Open

Abstract

acute kidney injury chronic kidney disease gene expression hemodialysis sepsis
A systems biology approach was used to comprehensively examine the impact of renal disease and hemodialysis (HD) on patient response during critical illness. To achieve this, we examined the metabolome, proteome, and transcriptome of 150 patients with critical illness, stratified by renal function. Quantification of plasma metabolites indicated greater change as renal function declined, with the greatest derangements in patients receiving chronic HD. Specifically, 6 uremic retention molecules, 17 other protein catabolites, 7 modified nucleosides, and 7 pentose phosphate sugars increased as renal function declined, consistent with decreased excretion or increased catabolism of amino acids and ribonucleotides. Similarly, the proteome showed increased levels of low-molecular-weight proteins and acute-phase reactants. The transcriptome revealed a broad-based decrease in mRNA levels among patients on HD. Systems integration revealed an unrecognized association between plasma RNASE1 and several RNA catabolites and modified nucleosides. Further, allantoin, N1-methyl-4-pyridone-3-carboxamide, and N-acetylaspartate were inversely correlated with the majority of significantly downregulated genes. Thus, renal function broadly affected the plasma metabolome, proteome, and peripheral blood transcriptome during critical illness; changes were not effectively mitigated by hemodialysis. These studies allude to several novel mechanisms whereby renal dysfunction contributes to critical illness.

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Collaboration types
Industry collaboration
Domestic collaboration
Web of Science research areas
Urology & Nephrology
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