Abstract: TH-OR097
CKD in Pediatric Patients: From Targeted Proteomics to Network-Based Modeling of Inflammatory Signatures
Session Information
- Shaping Pediatric Kidney Disease: Developmental Insights, Stem Cell Systems, Novel Biomarkers, and More
October 22, 2026 | Location: Room 603, Convention Center
Abstract Time: 05:30 PM - 05:40 PM
Category: Pediatric Nephrology
- 1800 Pediatric Nephrology
Authors
- Van Wesemael, Pauline, Department of Pediatric Nephrology, Ghent University Hospital, Ghent, Belgium
- Vermeersch, Anne-Sofie, Laboratory of Pharmaceutical Biotechnology, Faculty of Pharmaceutical Sciences, Ghent University, Ghent, Belgium
- Glorieux, Griet Lrl, Department of Nephrology, Ghent University Hospital, Ghent, Belgium
- Van Nieuwerburgh, Filip, Laboratory of Pharmaceutical Biotechnology, Faculty of Pharmaceutical Sciences, Ghent University, Ghent, Belgium
- Perco, Paul, Delta 4 GmbH, Vienna, Austria
- Keska-Izworska, Kinga, Delta 4 GmbH, Vienna, Austria
- Kratochwill, Klaus, Delta 4 GmbH, Vienna, Austria
- Raes, Ann Marijke, Department of Pediatric Nephrology, Ghent University Hospital, Ghent, Belgium
- Collard, Laure, Department of Pediatric Nephrology, CHC Liège, Liège, Belgium
- Van Hoeck, Koen Jm, Department of Pediatric Nephrology, Antwerp University Hospital, Antwerp, Belgium
- Adams, Brigitte, Department of Pediatric Nephrology, University Hospital Leuven, Leuven, Belgium
- Godefroid, Nathalie, Department of Pediatric Nephrology, University Hospital Saint-Luc, Brussels, Belgium
- Eloot, Sunny, Department of Nephrology, Ghent University Hospital, Ghent, Belgium
- Snauwaert, Evelien, Department of Pediatric Nephrology, Ghent University Hospital, Ghent, Belgium
Background
Chronic low-grade inflammation, largely driven by organic metabolites that accumulate with deterioration of kidney function, plays a crucial role in the pathophysiology of pediatric chronic kidney disease (pCKD). Therapies interfering with the inflammatory signature in CKD are hypothesized to beneficially impact the outcomes of patients. pCKD, predominantly caused by congenital anomalies of kidney and urinary tract (CAKUT), represents a unique population to investigate the inflammatory signature of CKD without confounding inflammatory comorbidities as presented in adults.
Methods
A network-based molecular model of CAKUT was generated based on literature-derived proteins, publicly available omics data and protein-protein interaction data following established systems biology workflows. Differently expressed proteins (DEPs) were incorporated into the model. These DEPs were identified from plasma samples of children (0-18yo) with CKD stage 1-5D and age-matched controls, using the targeted OLINK Explore 384 Inflammation panel. Group comparison of normalized protein expression (NPX) values was performed using Welch's t-test (FDR <0.05, NPX change |>1|). Patients were selected from a Belgian multicentric pCKD biobank (recruited 2014-19).
Results
166 inflammatory proteins were significantly upregulated in CKD 1-5D (n=59) versus healthy children (n=24)(fig. 1a). The generated network-based CAKUT model consisted of 291 proteins, and the top 20 enriched molecular mechanisms were identified (fig. 1b). 11 of the DEPs were part of the CAKUT model or linked directly to core molecular mechanisms of CAKUT.
Conclusion
This study shows a prominent upregulation of inflammatory proteins in a pCKD cohort without confounding inflammatory comorbidities. 11 DEPs could be directly linked to CAKUT associated molecular mechanisms revealing close relations between different affected proteins in CAKUT. This systems biology molecular view of CAKUT/pCKD forms the basis to search for novel treatment options counterbalancing dysregulated mechanisms linked to inflammation in pCKD.
Fig 1: a. NPX CKD vs healthy; b. top 20 enriched pathways