ArticlePediatric nephrology (Berlin, Germany)2026
Neutrophil extracellular traps drive peritoneal inflammation and tissue remodeling in pediatric peritoneal dialysis.
Article in Pediatric nephrology (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Changing prognostic significance of peritoneal transport status in contemporary incident peritoneal dialysis patients.Clinical kidney journal · 2026Article
- Host-Pathogen Crosstalk in Pediatric Peritoneal Dialysis-Associated Peritonitis: Molecular Mechanisms Driving Peritoneal Membrane Remodeling.International journal of molecular sciences · 2026Review
- The peritoneal immune niche in peritoneal dialysis-induced membrane failure: macrophages, neutrophils and extracellular trap biology.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundPeritoneal dialysis (PD) sustains children with chronic kidney disease stage 5 (CKD5) but promotes peritoneal membrane remodeling. Neutrophil extracellular traps (NETs) orchestrate antimicrobial defense and sterile inflammation; their involvement in PD-induced transformation is unknown.
methodsForty-five children were enrolled in the International Pediatric Peritoneal Biobank. Peritoneal biopsies taken at PD initiation and after ≥ 12 months of low-glucose-degradation-product PD were compared with surgical biopsies from non-uremic peers. Histomorphometry quantified microvessel density, submesothelial thickness, leukocyte infiltration, collagen I/III, and NET markers (citrullinated histone H3, neutrophil elastase, myeloperoxidase). Dialysate and plasma collected every 2 months for 18 months were assayed for cell-free DNA, NET proteins, DNase1, and DNase1L3.
resultsAfter chronic PD, the peritoneum displayed doubled microvessel density, tripled submesothelial thickness, and marked immune-cell infiltration (all p < 0.01). NET structures were prominent in tissue, while dialysate and plasma concentrations of cell-free DNA, citrullinated histone H3, neutrophil elastase, and myeloperoxidase increased two- to fourfold versus baseline (p < 0.05). DNase1 levels correlated with membrane thickness (r = 0.46, p = 0.003) and DNase1L3 with vascular density (r = 0.51, p = 0.001), suggesting limited compensatory NET clearance.
conclusionsChronic PD elicits NET-driven sterile inflammation that parallels structural remodeling of the pediatric peritoneum. Supplementing PD fluids with exogenous NET-degrading enzymes may preserve membrane integrity and prolong PD suitability in children.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.