Peritoneal dialysis (PD)-associated peritonitis in children represents a complex interplay between microbial virulence, host immune activation and progressive peritoneal membrane remodeling. It should not be viewed solely as an acute infectious episode, but as a process unfolding within a chronically conditioned immune environment shaped by prolonged exposure to glucose-based dialysis solutions, oxidative stress and persistent biofilm formation on the Tenckhoff catheter. Mesothelial cells act as immunologically active sentinel cells, recognizing pathogen-associated molecular patterns through Toll-like receptors and related innate pathways. Subsequent activation of nuclear factor kappa B, inflammasome signaling and neutrophil extracellular trap formation further amplifies local inflammatory responses. Repeated inflammatory stimulation promotes mesothelial–mesenchymal transition, angiogenesis and extracellular matrix deposition driven by transforming growth factor beta 1 and interconnected profibrotic networks. In pediatric patients, prolonged PD vintage during critical stages of growth may intensify cumulative structural injury and increase the risk of ultrafiltration failure or encapsulating peritoneal sclerosis. Emerging strategies targeting inflammation, fibrosis and biofilm persistence, together with earlier molecular risk detection, may support preservation of the peritoneal membrane. A unified host–pathogen framework may therefore deepen pathophysiological insight and facilitate more individualized therapeutic strategies in pediatric PD.
Dotis et al. (Mon,) studied this question.