title: Peritoneal defence--lessons learned which apply to diabetes complications.
abstract: Peritoneal dialysis (PD) and diabetes mellitus share the high glucose concentration in the cell microenvironment. This has led to the suggestion that they may also share pathogenic pathways of cell and tissue injury. Hypotheses have been formulated on the pathogenesis of peritoneal injury in the course of PD that take into account knowledge of the mechanisms of tissue injury in diabetes patients. More recently, research on the pathways of PD complications has uncovered potentially novel mediators of diabetes complications. Accelerated leucocyte apoptosis has been identified as a cause of impaired peritoneal antibacterial defence in PD, which may lead to new therapeutic interventions. In this regard, interference with leucocyte apoptosis by the use of caspase inhibitors may accelerate the clearance of bacteria such as Staphylococcus aureus, which cause significant morbidity in both PD and diabetes patients. Evidence suggests that glucose degradation products in PD solutions accelerate leucocyte apoptosis. In particular, 3,4-di-deoxyglucosone-3-ene (3,4-DGE) accounted for most, if not all, the cytotoxicity of PD fluids against neutrophils and lymphocytes. Interestingly, 3,4-DGE also induces apoptosis in cells, such as renal epithelium, from organs that are targets of diabetes complications. This raises the possibility that apoptosis induction by glucose metabolites that are the key participants in PD complications may underlie the pathogenesis of some features of diabetic tissue injury.
authors.affiliation: Unidad de Diálisis, Fundación Jiménez Díaz, Av Reyes Católicos 2, Madrid 28040, Spain.
authors.forename: Beatriz
authors.initials: B
authors.lastname: Santamaría
authors.forename: Ana
authors.initials: A
authors.lastname: Sanz
authors.forename: Pilar
authors.initials: P
authors.lastname: Justo
authors.forename: Marina
authors.initials: M
authors.lastname: Catalán
authors.forename: Maria Dolores
authors.initials: MD
authors.lastname: Sánchez-Niño
authors.forename: Alberto
authors.initials: A
authors.lastname: Benito
authors.forename: Corina
authors.initials: C
authors.lastname: Lorz
authors.forename: Belén
authors.initials: B
authors.lastname: Marrón
authors.forename: Alberto
authors.initials: A
authors.lastname: Ortiz
mesh_terms: D000818:Animals; D017209:Apoptosis; D048909:Diabetes Complications; D015314:Dialysis Solutions / Q000633:toxicity*; D005947:Glucose / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000378:metabolism / Q000633:toxicity; D006801:Humans; D010530:Peritoneal Dialysis; D010537:Peritoneum / Q000473:pathology*; D010538:Peritonitis / Q000209:etiology
chemical_list: D015314:Dialysis Solutions; D017127:Glycation End Products, Advanced; D005947:Glucose