Fig. 3.

Combination of bioincompatibility of current peritoneal dialysis (PD) fluids in combination with infection and chronic inflammation results in abnormal peritoneal repair processes. Oxidative stress, senescence, and inadequate cellular stress responses are pathomechanisms that mediate glucose-related toxicity, enhance chronic inflammation, and reduce peritoneal host defence, thereby contributing to a vicious circle. Epithelial mesenchymal transdifferentiation (EMT) further mediates peritoneal membrane damage by peritoneal fibrosis and angiogenesis, ultimately resulting in technical failure of PD. These pathomechanisms might be amenable to therapeutic interventions by specific counteracting compounds