Abstract
During long-term peritoneal dialysis (PD) the peritoneal membrane underlies processes of structural and functional reorganization mediated by high glucose and reactive glucose metabolites that are contained in PD solutions; this process is accompanied by increasing fibrosis. Mechanistically, the peritoneal damage is triggered by the interaction of advanced glycation end-products with their receptor; this is true for rodents as well as for humans. With this knowledge interventional strategies can be tested in rodent models, among them are the lipid soluble vitamin B1 analogue benfotiamine (BF) or detoxifying enzymes such as glyoxalase. Of additional interest is the finding that PD fluids do not only cause local but also systemic damage, in particular renal and cardiovascular. In the case of kidney damage, the intervention with BF was also successful. Taken together, PD can be regarded as a local model for long-term diabetes together with systemic aspects of damage.
Key words
diabetes - reactive glucose metabolites - glucose degradation products - advanced glycation end-products - peritoneum - local damage
