Last update:
11-Jun-2025

Despite the theoretical acknowledgment that dysregulation of calcium homeostasis plays a substantial role in the development of peritoneal dialysis (PD)-related peritonitis, the supporting evidence for this hypothesis is currently constrained and lacks comprehensive validation. The dysregulation of calcium homeostasis, a critical physiological process, can instigate a cascade of diverse biochemical and pathological alterations within the body, significantly heightening susceptibility to PD-related peritonitis. When calcium regulation becomes imbalanced, it can precipitate secondary hyperparathyroidism, leading to an abnormal accumulation of calcium within cells. Simultaneously, heightened phosphates can trigger an elevation in fibroblast growth factor 23 (FGF23) levels. These interconnected disturbances in calcium metabolism may synergistically contribute to the development of peritoneal fibrosis and vascular calcification. The intricate interplay of these factors not only disrupts the delicate equilibrium of cellular environments but also sets the stage for an increased risk of PD-related peritonitis, underscoring the intricate relationship between calcium dysregulation and the pathogenesis of PD-related peritonitis. In conclusion, the pivotal role of calcium homeostasis dysregulation emerges as a critical factor intricately intertwined with the pathogenic processes, exerting a fundamental influence on the development and progression of PD-related peritonitis.

Key words: Calcium, Pathogenesis, Peritoneal dialysis, Peritonitis, Phosphate.